Talk:Alzheimer's disease/Archive 12

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See also sections

First they are not recommended per WP:MEDRS. Second if we include Braak staging somewhere in the article what should we say about it? Maybe on the subapge Biochemistry of Alzheimer's disease Doc James (talk · contribs · email) 14:34, 19 August 2015 (UTC)

"See also" sections are sometimes useful as an indication of material missing from an article. That might be the case here. It seems to me that this article ought to make it clearer that AD can't be diagnosed definitively without examining brain tissue, which is usually not possible until after death. When the postmortem diagnosis is made, the severity of the disease is assessed using Braak staging. (I assume; this is not an area of expertise for me.) Looie496 (talk) 15:25, 19 August 2015 (UTC)

We have the sentence "Examination of brain tissue is needed for a definite diagnosis"

"See also" sections often appear to be a place to park stuff that is only tangentially related. The source seems more important in PD Doc James (talk · contribs · email) 15:37, 19 August 2015 (UTC)

If what Looie says is true we should always be aiming to remove these sections, they are only useful when they are being deleted. I'll do this from now on generally, not fond of see also. There should always be enough links in the article of interest to NOT require this section but to integrate its orphaned members♫ SqueakBox talk contribs 15:47, 19 August 2015 (UTC)

This is a Featured Article, and FA's generally shouldn't need a See Also section. But in a Stub or Start-class article where important information is missing, a See Also section can be a reasonable expedient for an editor who isn't up to the task of adding proper text. I agree that they are often misused, though. Looie496 (talk) 16:54, 19 August 2015 (UTC)

My own rule of thumb is that if the article has lots of links it doesnt need a see also section, and this thread is encouraging me to be bold; in starter articles an attempt should be made to integrate the see also links into the text but bold removal isnt required. ♫ SqueakBox talk contribs 17:44, 19 August 2015 (UTC)

SqueakBox, stating that See also sections "are only useful when they are being deleted" and "if the article has lots of links it doesnt need a see also section" is not correct. WP:See also is clear about See also sections being beneficial and when they should be used. An article having a lot of links doesn't mean that it shouldn't have a See also section. Often, the See also section contains links that should be in the body of the article. So instead of removing a See also section, as you did in this recent case, which brought me to this Alzheimer's disease discussion when looking at your latest contributions, you should be seeing how you can incorporate those links into the body of the article, and then remove the section. Other times, a See also section has links that are "only indirectly related to the topic of the article," and, per WP:See also, this is fine. Flyer22 (talk) 04:33, 20 August 2015 (UTC)

If I had thought any of those links were wroth integrating into the human section which is already unbalancing the article in favour of humans, I would have done so. Perhaps there should be a separate article for human secondary sexual characteristics where all those links could indeed be merged into the text. For me those arent though the links I would expect to see on a more general article on secondary sexual characteristics, but this isnt the place to discuss any of that. ♫ SqueakBox talk contribs 04:50, 20 August 2015 (UTC)

SqueakBox, we should ideally only split content into separate articles when needed. Per WP:Spinout and WP:No split, I hate unnecessary spinout articles. If the Secondary sex characteristic article needs more non-human animal content, then it should be expanded to include that, not split so that humans have a page just for them. I'd rather you discuss this matter, either at that article's talk page, at WP:Anatomy and/or at WP:Biology before making such a split. When I see unnecessary splits, I tend to suggest and/propose a WP:Merge. Flyer22 (talk) 05:34, 20 August 2015 (UTC)

Potential additions for "Early Diagnosis" section of page

A Cochrane review published in 2014 looked at studies which analyzed the levels of cerebrospinal fluid for amyloid-beta proteins in patients with mild cognitive impairment. This systematic review determined that these levels are not an accurate marker for the development and diagnosis of Alzheimer's disease in these patients who are exhibiting symptoms of memory loss. --Rhoner (talk) 22:22, 13 October 2015 (UTC)

References

Recent report on new potential cause

Published in nature on Oct 15 http://www.nature.com/articles/srep15015; this article suggests that there is evidence for a fungal infection in AD patients, perhaps even as the cause. It is of significant interest as clinical trials could offer the possibility for a new vector for treatments. Worth a line in the cause section? 151.224.234.183 (talk) 19:32, 19 October 2015 (UTC)

spirochetes in ~ 90% of Alzheimer’s patients' CNS, but virtually absent in healthy age-matched controls

Research has shown that some common bacteria are consistently detected in the central nervous system of Alzheimer’s patients.1

Doctors from the International Alzheimer Research Center in Switzerland published a study indicating a high probability of a causal relationship, not just an association, between spirochete infections and Alzheimer’s disease.

What they discovered was pretty amazing. They found spirochetes in about 90% of Alzheimer’s patients, while the bacteria were virtually absent in healthy age-matched controls.1 (emphasis added)

More, with possible prevention/treatment, both pharmaceutical and herbal, with more references at: http://blog.lifeextension.com/2013/12/is-alzheimers-caused-by-infection.html

Someone w/medical training should look into this for possible inclusion.

Phantom in ca (talk) 05:38, 3 December 2015 (UTC)

I just saw a comment left at the bottom of the brief article linked above:

Alzheimer's and Neuroborreliosis studies commenced in 1985 with my papers describing the cultivation of borrelia and the identification of borrelia in autopsy tissues from Dr. Geroge Glenner's Alzheimer Disease Brain bank. These reports were published in JAMA, Human Pathology, and The Annals of the New Academy of Sciences in 1986, 1987, 1988. Respectfully, Alan B.MacDonald Md

Phantom in ca (talk) 05:44, 3 December 2015 (UTC)

Added a sentence on this [1] Doc James (talk · contribs · email) 08:06, 3 December 2015 (UTC)

New text

This was added "There are treatments that stop or reverse its progression" support by this [2]. First that is a primary source and second I am not seeing were it says reverses progression?

The prior source in Mar 2015 says "There is no treatment currently available to cure dementia or to alter its progressive course."[3] Doc James (talk · contribs · email) 08:59, 9 January 2016 (UTC)

--"Combining memantine and donepezil had an additive effect". Suggests that it might be helpful in reversing temporarily the symptoms of Alzheimers disease? --RuleTheWiki (talk) 08:18, 14 January 2016 (UTC)

Not sure what that means. It does not appear to state that it reverses symptoms. We need a better source IMO. Doc James (talk · contribs · email) 09:32, 14 January 2016 (UTC)

Good summary article from New England Journal of Medicine (2004)

• Cummings JL (2004 Jul). "Alzheimer's Disease". N Engl J Med. 351 (1): 56–67. doi:10.1056/NEJMra040223. PMID 15229308. {{cite journal}}: Check date values in: |date= (help)

- — Preceding unsigned comment added by Ottestad (talk • contribs) 02:11, 29 December 2010 (UTC)

Potential addition for "Medications" section of page

A systematic review showed that memantine and rivastigmine are effective for improving the behavioral and psychological symptoms of dementia without causing any major side effects in many patients.

References

Rhoner (talk) 18:58, 4 December 2015 (UTC)

The source you cite is not a systematic review. It is a primary research study that appeared in the Journal of Alzheimer's Disease, see PMID 24164733. Google Scholar doesn't show any citations of that study by Cochrane Reviews either. Looie496 (talk) 20:34, 4 December 2015 (UTC)

Neuroangiogenesis

Hi, Just wanted to check whether this page's editor(s) felt that Neuroangiogenesis merited a link on the angiogenesis page? And if this should be in the 'See Also' section or have its own section on the page or just a link? Let me know your thoughts anyway. Stinglehammer (talk) 11:08, 1 March 2016 (UTC)

I haven't edited this page, but I'll express an opinion anyway. It is always preferable to have text that explains the relevance of a related topic rather than just a See Also link -- however a See Also link is a reasonable expedient if an editor feels that a topic is clearly relevant but doesn't feel up to the task of writing text that explains why. I doubt that a section of text is justified, because this is a pretty minor topic, but if a See Also link is justified then a sentence at some appropriate point should be too. Looie496 (talk) 14:33, 1 March 2016 (UTC)

Potential addition for "Research Directions" section

A systematic review showed that microRNA could provide a relatively quick and easy method for detection of Alzheimer's Disorder. Further research is required to classify miRNA categories as well as isolate specific miRNA combinations associated with AD.

References

Dameister22 (talk) 02:16, 9 March 2016 (UTC)

there are zillions and zillions of potential diagnostics for AD. This is not helpful content. Jytdog (talk) 02:43, 9 March 2016 (UTC)

Potential additions to the "Medication" section

A systematic review has found that idalopirdine, in conjunction with donepezil had a positive effect on cognitive functioning in patients with moderate Alzheimers.

References

Dameister22 (talk) 02:16, 9 March 2016 (UTC)

the source there is not a review. it is a primary source. Please see WP:MEDRS. Jytdog (talk) 02:40, 9 March 2016 (UTC)

Another systematic review had findings that showed atypical antipsychotics such as risperidone and olanzapine yielded positive results in reducing aggression in Alzheimer's patients and that risperidone also improved psychosis. While these results are promising, the authors suggested that these treatment options only be used in extreme settings where the patient may cause harm to his/herself and others.

References

Dameister22 (talk) 02:35, 9 March 2016 (UTC)

Please always provide the PMID when you create a citation in Wikipedia. If you do nothing else, please use that. It is really important to us. The PMID here is PMID 16437455. This is a pretty old source - 10 years old, and there are much more recent ones - see here.

Also, there is already content in this article about antipsychotics. It is not clear how the new content would fit with that.... Jytdog (talk) 03:04, 9 March 2016 (UTC)

It says "Evidence suggests that risperidone and olanzapine are useful in reducing aggression and risperidone reduces psychosis, but both are associated with serious adverse cerebrovascular events and extra-pyramidal symptoms. Despite the modest efficacy, the significant increase in adverse events confirms that neither risperidone nor olanzapine should be used routinely to treat dementia patients with aggression or psychosis unless there is marked risk or severe distress. "[4]

And we use to support this in the article already "Atypical antipsychotics are modestly useful in reducing aggression and psychosis in people with Alzheimer's disease, but their advantages are offset by serious adverse effects, such as stroke, movement difficulties or cognitive decline" Doc James (talk · contribs · email) 03:08, 9 March 2016 (UTC)

Tau Axis Hypothesis

Recent research has proposed a new Tau Axis hypothesis that integrates both the Tau and Amyloid hypotheses. It argues that the two proteins may have an interactive and synergistic effect in the development of Alzheimers Disease.

References

— Preceding unsigned comment added by Bsaway (talk • contribs) 03:47, 9 March 2016 (UTC)

we write in English not German - we don't capitalize nouns in English. 5 years ago is not recent. Please provide PMIDs in your citations. Thanks. Content from this source may be useful in the Research section... Jytdog (talk) 04:07, 9 March 2016 (UTC)

Galantamine

We would like to add a citation to a Cochrane Review here. I found it using TRIP, and it summarizes multiple studies looking at galantamine, concluding that the effect is positive. This looks like it may be a better source than the two used here -- one is in a small journal and may be a primary source; neither is a Cochrane systematic review. It is older than the others, which seems like the potential issue. This is the text that we would like to edit:

"The benefit from their use is small.[166][167] No medication has been clearly shown to delay or halt the progression of the disease."

This is the source I would like to try to add:

Loy C. & Schneider L. (2006). Galantamine for Alzheimer’s disease and mild cognitive impairment. Cochrane Database of Systematic Reviews, Issue 1. Art. No.: CD001747. DOI: 10.1002/14651858.CD001747.pub3.

Thanks for considering! Slinfree (talk) 22:00, 8 March 2016 (UTC)

this is PMID 16437436. it is a ten year old source. if you search pubmed for reviews, you find more recent ones. PMID looks especially useful as it looks at the drugs together. Jytdog (talk) 06:13, 9 March 2016 (UTC)

Diagnosis

Regarding the diagnosis of Alzheimer's Disease, I believe I have found more recent research (from 2015) about PET scans and the early diagnosis of AD from the Cochrane Database of Systematic Reviews.

It would be worth considering citing this source:

Smailagic N., Vacante M., Hyde C., Martin S., Ukoumunne O., & Sachpekidis C. (2015). 18F-FDG PET for the early diagnosis of Alzheimer’s disease dementia and other dementias in people with mild cognitive impairment (MCI). Cochrane Database of Systematic Reviews, Issue 1. Art. No.: CD010632. DOI: 10.1002/14651858.CD010632.pub2.

(Instead of this source:)

Schroeter ML, Stein T, Maslowski N, Neumann J. Neural Correlates of Alzheimer's Disease and Mild Cognitive Impairment: A Systematic and Quantitative Meta-Analysis involving 1,351 Patients. NeuroImage. 2009;47(4):1196–1206. doi:10.1016/j.neuroimage.2009.05.037. PMID 19463961.

Thank you for your consideration! Slinfree (talk) 00:37, 9 March 2016 (UTC)

I found a more recent source that explains the use of plasma and cerebrospinal fluid amyloid beta for the early diagnosis of AD using Trip database from the Cochrane Database of Systematic Reviews. Perhaps we could consider replacing citation 127:

Marksteiner J, Hinterhuber H, Humpel C. Cerebrospinal Fluid Biomarkers for Diagnosis of Alzheimer's Disease: Beta-amyloid(1–42), Tau, Phospho-tau-181 and Total Protein. Drugs of Today. 2007;43(6):423–31. doi:10.1358/dot.2007.43.6.1067341. PMID 17612711.

with this more recent source (from 2014):

Ritchie C., Smailagic N., Noel-Storr A.H., Takwoingi Y., Flicker L., Mason S.E., & McShane R. (2014). Plasma and cerebrospinal fluid amyloid beta for the diagnosis of Alzheimer’s disease dementia and other dementias in people with mild cognitive impairment (MCI). Cochrane Database of Systematic Reviews, Issue 6. Art. No.: CD008782. DOI: 10.1002/14651858.CD008782.pub4.

Thank you! Slinfree (talk) 00:51, 9 March 2016 (UTC)

content in wikipedia is actually based on the sources. it would be very useful for you to read the new sources and see if there are any changes needed to the content, and if there are, make them. if the state of the science hasn't changed, then all you will indeed do is replace the source. but never just plug sources in please. Jytdog (talk) 06:26, 9 March 2016 (UTC)

J. of Alzheimer's Disease editorial calls for studies re. infections as AD causative agents

Perhaps they'll start a new category of diseases: KTDs (kissing transmitted diseases)

Here's a NY Post article re. the editorial: http://nypost.com/2016/03/15/could-a-virus-cause-alzheimers-disease/

Here's a direct link to the Journal of Alzheimer's Disease editorial: http://content.iospress.com/articles/journal-of-alzheimers-disease/jad160152

I'll let someone else (hat tip to Doc James ;) ), add this to the main article if appropriate.

Phantom in ca (talk) 03:11, 16 March 2016 (UTC)

Under other hypothesis we mention "Herpes simplex virus type 1 has been proposed to play a causative role in people carrying the susceptible versions of the apoE gene.[67] Chronic bacterial infections have also been proposed as a potential risk factor.[68]" Doc James (talk · contribs · email) 03:31, 16 March 2016 (UTC)

I wasn't sure if you'd want to add it as another footnote since it marks a "sea change" (or at least calls for a sea change), in the direction of AD research, turning infectious agents from a minor, ignored area of research to a major focus.

BTW thanks for all your work on the article and making it worthy of being a featured article. Phantom in ca (talk) 04:27, 16 March 2016 (UTC)

Upon further reflection, I think that the editorial (with its 31 signature experts) should be cited as a footnote at the end of the Amyloid Hypothesis section (https://en.wikipedia.org/wiki/Alzheimer's_disease#Amyloid_hypothesis) because it is calling for abandoning the hypothesis that amyloid B is "the cause" of AD. That is the main point of it. The secondary point is to suggest changing the focus of future AD research to possible infectious agents causing AD.

Extra: I saw this and thought I'd pass it along. I'll leave it to the Wiki AD experts decide which article on AD (familial, sporadic, late onset), it might help. http://www.j-alz.com/editors-blog/posts/early-and-late-onset-alzheimers-disease-two-different-entities Phantom in ca (talk) 22:48, 16 March 2016 (UTC)

BMAA theory

I added this under the section: 'Other hypotheses': "The non-proteinogenic amino acid beta-Methylamino-L-alanine (BMAA) may serve as an environmental trigger for AD. BMAA is produced by cyanobacteria which are common constituents of algal blooms in eutrophic waters." I'm not sure if it needs further discussion? — Preceding unsigned comment added by Alandmanson (talk • contribs) 09:05, 18 March 2016 (UTC)

Yes, you added that here. That was sourced to what we call in Wikipedia a "primary source" and a press release. Please do see our guideline for sourcing content about health, WP:MEDRS, and particularly the section WP:MEDREV which talks exactly about this situation. After you added that I reviewed the section and trimmed that and a bunch of other content that was there, that was based only on primary sources. If you want to understand better why we follow MEDRS, please see the essay (which I mostly wrote) WP:Why MEDRS? Jytdog (talk) 17:22, 18 March 2016 (UTC)

Reading

change ((reading)) to ((Reading (process)|reading))

 Done I'm not sure this really needs to be wikilinked, but since it already was, we might as well use the correct link. Looie496 (talk) 14:46, 24 March 2016 (UTC)

Propose inclusion of Bredesen research on reversing Alzheimer's/MCI and dividing Alzheimer's in subtypes

I think it would be useful to at least mention the research of Dale Bredesen at UCLA: http://www.eastonad.ucla.edu/about-us/faculty-and-staff/item/bredesen-dale-e-md

In 2014 he reports in Aging, a peer-reviewed journal with a very large impact factor (they claim the highest in field I believe) and several publications from Nobel laureates, that in a small clinical trial he was able to reverse memory loss in 9 of 10 patients with Alzheimer's/MCI (http://www.impactaging.com/papers/v6/n9/full/100690.html). (The 10th may have been too far along.) As I understand it, his approach is to analyze the factors involved in brain health, determine which of those factors a given patient appears weak in, and use existing treatments on each of those factors. I think his underlying hypothesis is that Alzheimer's is not so much a single-cause illness as severe dysfunction of the brain caused by various factors. Hence we have been unable to find any sort of "silver bullet". He is working on a larger trial now, having at least started work on about 70 patients, https://www.mpicognition.com/wp-content/uploads/2016/01/IMCJ2015.pdf.

As best as I am aware, no one has made any attempt to contradict, overturn, or even had meaningful criticism of this research. He has been working in this field over 30 years and does not seem to be into self-aggrandizement.

In 2015 he reports in the same journal that "metabolic profiling" reveals 3 subtypes of Alzheimer's, which I can attempt to roughly characterize as "inflammatory" (similar to Perlmutter claims?), "non-inflammatory", and special/young. I'm not an MD or even a biologist; please see his paper for details: http://www.impactaging.com/papers/v7/n8/pdf/100801.pdf

There are now two companies trying to commercialize his protocol: Muses Labs (which he has disaffiliated with), and MPI Therapeutics: https://www.mpicognition.com/.

Perhaps this should only be mentioned on the Alzheimer's Disease Research page. I did not find any mention of it there either; it sounds like it has not been updated in a while. This functional/programmatic approach is entirely different from the apparent "single-approach" approaches mentioned on the page.

Full disclosure: I have no financial or personal stake in Bredesen, the companies, or any form of Alzheimer's/MCI work. I stumbled across it a few months ago and have found very few people know about it despite its possible importance. My general practitioner has given out the paper to at least one person I know, even if she forgot I gave it to her.  :-)

Paultparker (talk) 15:44, 16 April 2016 (UTC)

We base our articles on review articles typically. Doc James (talk · contribs · email) 17:22, 16 April 2016 (UTC)

Retrogenesis

Two sentences about Retrogenesis were added in under the other hypothesis section. Retrogenesis is a new hypothesis that is under investigation to try and explain AD. Retrogenesis was linked in order to make the Retrogenesis page no longer an orphan page. Kclarke11 (talk) 19:15, 26 April 2016 (UTC)

Description of Disease and Diagnosis

There are a couple of suggestions I would like to make for this article:

1) Alzheimer's is characterized by a change to the baselines cognitive processes, meaning if the person always had memory problems, having memory problems as this person ages is normal. If, however, the person had great memory all of his or her life, but then later loses the ability to achieve memory feats of similar caliber, this is a change from the baseline, and thus a way to identify Alzheimer's disease. I do not think the article clearly makes this distinction and I believe it to be important to include because some memory loss as people age is normal, it is a change from this baseline that is unhealthy aging.

2) There have been several studies conducted about the diagnosis of Alzheimer's through language. One such study that I think would be valuable to add to such a Wikipedia page is the nun study. This study used nuns as the subjects and compared written essays from the nuns when they were in their 20's to when they were in their 80s. The results of this study indicate that a change in language complexity and use over time can be an indication of Alzheimer's disease. More specifically, if someone in their 20s was an extremely complex writer that utilized new words and unique vocabulary, but 50 years later uses high frequency words and less complex words, this decline in language may be a significant predictor of Alzheimer's.

Citation for Nun Study:

• Kemper, Susan; Greiner, Lydia; Marquis, Janet; Prenovost, Katherine; Mitzner, Tracy (2001). "Language Decline Across the Life Span: Findings From the Nun Study" (PDF). Psychology and Aging. 16 (2): 227–239.

Zoeberk (talk) 20:11, 16 April 2016 (UTC)

We source content about health in Wikipedia according to WP:MEDRS, which means review articles published in the biomedical literature or statements by major health authorities. We keep that standard for many, many reasons. But in any case, the source you bring is not OK per MEDRS. Jytdog (talk) 21:49, 16 April 2016 (UTC)

I like the idea of adding the nun study. I would include a link to the wikipedia article about the nun study. Also, in that wiki article and in the summary of the paper, it talks about how the linguistic density of the nuns' writing in their 20s was a predictor for Alzheimer's disease in old age. However, in your summary, you talk about how their writing from their 20s was compared with their writing in their 80s, and the change in writing was the important factor predicting Alzheimer's. I remember learning your version in class too, so I'm not sure which version is correct. I would look into that.Psy250 jes85 (talk) 01:27, 1 May 2016 (UTC)

Does the following citation comply with Wikipedia standards?

"Landmark Study Links Cognitive Ability of Youth with Alzheimer's Disease Risk Later in Life." National Institute on Aging. U.S. Department of Health and Human Services, 20 Feb. 1996. Web. 19 Apr. 2016. <https://www.nia.nih.gov/newsroom/1996/02/landmark-study-links-cognitive-ability-youth-alzheimers-disease-risk-later-life>.

Sowallabear (talk) 00:26, 20 April 2016 (UTC)

Not really, it is a dated news release about a primary study. However, that study has been widely cited, including in PMC 4674580, which is a 2015 review. We should go to the reviews for our sources, as explained at WP:MEDRS.LeadSongDog come howl! 14:21, 20 April 2016 (UTC)

I think I have found a good review paper that follows the proper criteria:

References

Zoeberk (talk) 21:31, 20 April 2016 (UTC)

Your addition regarding the Nun study is insightful. It is significant and relevant to the article because it provides one possible way to help identify Alzheimers, provided there is enough writing evidence for the person. Additionally, your addition provides an important qualification regarding Alzheimers: some degradation of memory is normal as one ages, and should not be confused with Alzheimers. For someone looking at the article for help/clarification, seeing this addition would hopefully dispel issues with people rushing to conclusions. Redmach197 (talk) 00:49, 2 May 2016 (UTC)

nun study

here is the content about the nun study, which I pulled from the article and put here.

In the Nun Study, a study conducted on a group of American Roman Catholic nuns, autobiographical essays written were compared from when they were in their 20's to when they were in their 80's. A change in language complexity and use over time indicated Alzheimer's disease. More specifically, if someone in their 20s was an extremely complex writer that utilized new words and unique vocabulary, but 50 years later uses high frequency words (i.e. words that are used very often such as "the") and less complex words, this decline in language may be a predictor of Alzheimer's. Alzheimer's is characterized as a change to baseline cognitive processes, not necessarily a decline in memory or language, as these declines are normal with healthy aging.

References

Some issues with this:

• Nice job getting a review from which to source this. It is an 8 year old review which is older than we prefer per WP:MEDDATE but it is a review.
• This is a high level article and in this section, which discusses things also at a high level, the addition of discussion of this one study sticks out as arbitrary.
• Most importantly what the source actually says is "These researchers have demonstrated that text-level writing abilities in early adulthood are a strong predictor of subsequent onset of dementia or mild cognitive impairments" In other words, it is not the writings from late in life that are diagnostic, but rather, the early writings. The content says that the decline in writing is predictive.
• Every diagnostic or prognostic test is evaluated in two main ways: 1) how sensitive is it? (in other words, does it pick up the condition every tiime? In other words, what is the rate of false negatives?) and 2) how specific is it? (in other words, am i testing for a lot of things, or just one thing? in other words, what is the rate of false positives?) The source makes it clear that this is a potential marker for dementia, MCI, and AD. In other words, unlikely to specific , at all. There is nothing about that in the content.
• Practically speaking, I am not sure what the value is, of an evaluation of written language complexity in early adulthood nor what you would do with this if confronted by an older person who was apparently beginning to have dementia, and you needed a differential diagnostic.
• I would be interested in seeing what weight more recent reviews give to the Nun study. Am looking now.

So I am opposed to this addition to this FA. Jytdog (talk) 02:17, 2 May 2016 (UTC)

this 2014 review on diagnostics for early AD doesn't mention anything like looking at written linguistic complexity, nor does this 2013 US preventative services task force screening-for-AD recommendations. Jytdog (talk) 02:55, 2 May 2016 (UTC)

Diagram of Alzheimers

After reading the first section and before scrolling down to more, the diagram of a regular persons brain and a person with Alzheimer's disease caught my attention. Not that we need to know what it looks like to have Alzheimers but the diagram is quite interesting and provides readers with more. TJ3Rahming (talk) 23:22, 2 May 2016 (UTC)

Age of onset figure Suggestion

Age of onset for early and late onset Alzheimer's disease.

I would like to add a figure portraying the age of onset probabilities for early and late onset Alzheimer's. When reviewing the article, it seemed to me that this is a topic that people likely have an interest in (well, at least those approaching these age ranges). Any thoughts on adding this image? Text changes would be minor - just mentioning early and late onset together in one place and adding file.scirp.org/Html/5-2440004_28635.htm the article where this data came from] to that sentence.

References

McortNGHH (talk) 15:15, 22 May 2016 (UTC)

Done Doc James (talk · contribs · email) 17:27, 22 May 2016 (UTC)

brain infection as real cause of AD, amyloid B as both effect (brain's innate immune response) and secondary cause (inflammation)

New study talked about in SciAm: http://www.scientificamerican.com/article/antimicrobial-mechanism-gone-rogue-may-play-role-in-alzheimer-s-disease/ It glosses over how tau fits in.

The original article (Science Translational Medicine article by neurologists Rudolph Tanzi and Robert Moir), might be added to infection hypothesis of AD (and/or as contra to amyloid hypothesis). Just a FYI for DocJames to decide what to do with this. Phantom in ca (talk) 16:15, 27 May 2016 (UTC)

Original article is PMID 27225182 - study in mice and worms. This is primary and we can't use it now. Jytdog (talk) 21:00, 27 May 2016 (UTC)

Lancet seminar

doi:10.1016/S0140-6736(15)01124-1 JFW | T@lk 23:48, 30 July 2016 (UTC)

Curcumin positive human trials

Contrary to what this article claims there seems to be at least one human trial of curcumin showing a positive effect on Alzheimer's.

Eledex (talk) 23:45, 4 August 2016 (UTC)

--Eledex (talk) 23:45, 4 August 2016 (UTC)

We wait for reviews on topics per WP:MEDRS Doc James (talk · contribs · email) 21:29, 5 August 2016 (UTC)

Aducanumab

The following was added by User:Proxima Centauri in this dif with the edit note that it needs vetting. Sourcing is not OK so I moved it here... but maybe there is a MEDRS source that discusses this?

Preliminary human trials suggest the drug, Aducanumab may help but further research is needed.

References

-- Jytdog (talk) 19:14, 31 August 2016 (UTC)

This is biogen's drug that has been hyped in the media based on PhII clinical trials.... this field is a graveyard with many many Phase III failures. discussed in two reviews, PMID 27025652 and PMID 26990863 both from this year... Maybe worth a mention in the Research section but do we really want to track the pipeline of clinical (or preclinical??) drug candidates here? Jytdog (talk) 19:16, 31 August 2016 (UTC)

New study from American College of Nutrition

Suggestion to add this to 2 Cause 2.5 Other hypothesis

Western Diet Increases Alzheimer's Risk http://www.americancollegeofnutrition.org/content/western-diet-increases-alzheimers-risk — Preceding unsigned comment added by Adessio (talk • contribs) 12:56, 1 October 2016 (UTC)

That paper presents research, so is a primary source. Jytdog (talk) 17:40, 1 October 2016 (UTC)

External links modified

Hello fellow Wikipedians,

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2016 in Alzheimer Keep it Separate?

Is there a better place to put this topic, then here? Does wiki have threads that could be posted to a page such as this? My comments are taking up valuable real estate on an important wikipage.

Suggestions anyone?

I started a new wikipage called "2016 in Alzheimer". {I suppose it would have been better to call it "2016 in Alzheimer's disease")

The page was originally going to be deleted, though an editor rescued the page. Thank you!! Yet, the idea for my sponsor is now to merge the page into the main Alzheimer's disease page.

I was thinking that "2016 in Alzheimer" would be more of a subcategory for the main "science in 2016" page. "2016 in Alzheimer" could then be followed by "2017 in Alzheimer", "2018 in Alzheimer" and so on.

The "science in 2016" page is such a diffuse sprawling category that the main Alzheimer breakthroughs for any given year is almost completely obscured by everything else. What I thought I could do was link the BACE1 inhibitor entry that I posted for Novemeber 3 on the science in 2016 page to the 2016 in Alzheimer page. This way I could drive and direct to the main Alzheimer year page. This idea was edited out. I think linking out from the main 2016 in science page would make quite a bit of sense. This could be done for a multiple of subcategories.

It might be better for this wikipage to link out to the 2016 in Alzheimer page. This could help keep separated out and a separate year page would avoid much of the clutter and datedness that can arise when maintaining a lead page such as the main Alzheimer's page.CRISPYgeneedit (talk) 18:31, 3 November 2016 (UTC)

Merged to Alzheimer's_disease_research Doc James (talk · contribs · email) 06:38, 4 November 2016 (UTC)

Omega-3 fatty acids and AD

I added a couple of sentences into the Dementia article, and was thinking of updating the Alzheimer's Disease page with info from the same review. https://www.ncbi.nlm.nih.gov/pubmed/27063583 There is already a small section in this wiki article stating that, "In those already affected with AD adding docosahexaenoic acid (DHA), an omega-3 fatty acid, to the diet has not been found to slow decline.[155]"

Proposed new sentence: Omega-3 fatty acid supplements from plants and fish, and dietary docosahexaenoic acid (DHA) supplements, do not appear to benefit people with mild to moderate Alzheimer's disease.[155] + (Burckhardt, 2016)

I realize that DHA is an omega-3 fatty acid in fish oil and seaweed. It appears that many herbal supplement companies sell DHA in a more purified form as well, so I included both in the sentence.

Thanks, JenOttawa (talk) 01:31, 9 November 2016 (UTC)

Sure Doc James (talk · contribs · email) 11:14, 9 November 2016 (UTC)

Semi-protected edit request on 30 November 2016

There is an inverse relationship between Alzheimer's disease and cigarette smoking when the patient carries the Apolipoprotein E-ε4 (ApoE4) gene; there is a protective effect of smoking with carriers of the gene ApoE4.

References

-- Ch4314a (talk) 14:11, 30 November 2016 (UTC)

Old primary source therefore not done. Please see WP:MEDRS Doc James (talk · contribs · email) 20:31, 30 November 2016 (UTC)

no mention of Case Western U neuro

Prof Joe Foley, Cleveland OH USA 99.245.191.116 (talk) 23:50, 13 December 2016 (UTC)

new research published on link between Aluminum and AD

Here's a popularly written article giving overview and a link to study (J. Trace Elements in Med. & Bio.) at the end: http://www.hippocraticpost.com/mental-health/strong-evidence-linking-aluminium-alzheimers/

Phantom in ca (talk) 06:05, 22 December 2016 (UTC)

Not a suitable source per WP:MEDRS and we already discuss with better sources which find "The majority of researchers do not support a causal connection with aluminium." Doc James (talk · contribs · email) 06:19, 22 December 2016 (UTC)

agreed. Jytdog (talk) 06:39, 22 December 2016 (UTC)

Section on comorbidities?

It might be helpful to add a section on other diseases that may occur in patients with Alzheimer's disease more often than would be predicted based on risk factors such as age and smoking history. Diabetes is one example: "... around 80% of people with Alzheimer's disease also have some form of diabetes or disturbed glucose metabolism." Research at the University of Aberdeen suggests that Alzheimer's disease may initiate diabetes rather than the other way around, as previously assumed: "...we show [in a mouse model] that dysregulation in the brain can equally lead to development of very severe diabetes -- so again showing that diabetes doesn't necessarily have to start with your body getting fat -- it can start with changes in the brain." Original journal article in Diabetologia Tetsuo (talk) 01:52, 18 January 2017 (UTC)

References

Is this British English or an error? (in Medication section)

"Evidence also support the notion" Should that be "Evidence also supports the notion" ? Tetsuo (talk) 02:05, 18 January 2017 (UTC)

Prognosis

The Wikipedia article says, "The mean life expectancy following diagnosis is approximately six years." I am uncertain whether this is supported by the source article. According to the abstract, "The mean durations were: AD 5.7 years..." The abstract doesn't say "from diagnosis." My read is that the researchers identified a group of people with AD at various stages of progression, as opposed to newly diagnosed, and then watched them for six years to see if they died. I would appreciate other opinions.Tetsuo (talk) 03:43, 18 January 2017 (UTC)

Agree Imersion (talk) 14:46, 17 April 2017 (UTC)

Move request

The ICD 10 uses "Alzheimer disease" not "Alzheimer's disease". Any one object to changing?[5] @Doc James: JeanOhm (talk) 02:02, 26 April 2017 (UTC)

I support. But let's give it a few days for others to weigh in aswell. Doc James (talk · contribs · email) 02:04, 26 April 2017 (UTC)

I have always called it "Alzheimer's disease"....so have set up two cats below and we can get some sense of usage. Cas Liber (talk · contribs) 02:55, 26 April 2017 (UTC)

Oppose - In everyday usage it's always referred to as Alzheimer's. He or she has Alzheimer's. .. but that would not change even after a name change --Iztwoz (talk) 09:48, 26 April 2017 (UTC)

Full support to standardising the possessive -'s either way in medical disorder names. ICD-10 has decided on no possessive and this is a strong argument that I would support unless WP:COMMONNAME would override this in individual cases. — kashmiri ^TALK 12:54, 26 April 2017 (UTC)

I just looked at WP:COMMONNAME. "Everybody" says "Down's syndrome", and yet common name uses the correct "Down syndrome". JeanOhm (talk) 17:50, 26 April 2017 (UTC)

More from commonname "In determining which of several alternative names is most frequently used, it is useful to observe the usage of major international organizations, major English-language media outlets, quality encyclopedias, geographic name servers, major scientific bodies, and notable scientific journals"

"major international organizations" ICD no possessive

"quality encyclopedias" Britannaca no possessive

"major scientific bodies/notable scientific journals" medline no possesive

One of my favorite signs from Trump demonstrators was "Denied facts still exist". The possessives of alz and Parkinson should not be used in a formal presentation, IMHO. — Preceding unsigned comment added by JeanOhm (talk • contribs) 18:05, 26 April 2017 (UTC)

This talkpage is not the place to establish or interpret a general guideline. A wp:local consensus, even if it were formed at wt:WikiProject Medicine would not override wp:AT. There are many examples at List of eponymously named diseases both with and without the apostrophe. In this particular matter, polyglot products such as the ICD have a strong incentive to ignore the reality of English-language usage inconsistency: it makes translation more complex. However, even the quickest scan of cited titles in the Alzheimer's disease#References section show that there a remarkable consistency in the use of that apostrophe in the cited English-language sources. We should follow the sources. @JeanOhm:, if you look closer at the wp:COMMONNAME portion of wp:AT you might notice that its mention of Down syndrome is: (a) simply a wikilink to the corresponding article; and (b) is used in comparison to the much-less used term trisomy 21 rather than to Down's syndrome. Accordingly, it is an unconvincing example. LeadSongDog come howl! 18:52, 26 April 2017 (UTC)

@LeadSongDog: Well, let's see....maybe this is a more convincing argument. The List of eponymously named diseases, which you led me too, lists alz without the possessive. It then links to this article with the 's. A VERY low percentage of the diseases in that list are possessives. So, maybe this isn't the place to establish a guideline. It has been estabished at that list. As I wrote previously, "Denied facts still exist".JeanOhm (talk) 02:29, 27 April 2017 (UTC)

Wikipedia attempts to follow, not lead. Roughly 80% of publications on AD still use the possesive form. The trend in possessive usage varies between countries, journals, and diseases.

Thank you for finding that paper, LeadSongDog. Of the six diseases & syndromes that it investigates, Gaucher['s] disease does not fit my hypothesis. Harrison's Principles of Internal Medicine has a chapter on lysosomal storage diseases (chapter 432e), which does indeed describe "Gaucher disease". The other eponymous lysosomal storage diseases described (Tay–Sachs disease, Fabry disease, Niemann–Pick disease and Pompe disease) also avoid the possessive form. (Oddly, the index of the textbook indicates "Gaucher's disease".) It is worth remembering that the different chapters of Harrison's Principles are written by different (sets of) authors. Also, these diseases are rare, and not well-recognised by the general public. Axl ¤ [Talk] 16:52, 27 April 2017 (UTC)

Alzheimer's disease

1. The Alzheimer's Association (in USA)
2. healthdirect - gov't funded site in Australia
3. neuRA - UNSW research facility
4. Mayo clinic
5. Alzheimer's Society (in UK)
6. the NHS
7. Royal College of Psychiatrists

Alzheimer disease

1. ICD10
2. medline JeanOhm (talk) 17:45, 26 April 2017 (UTC)
3. Britannica.com JeanOhm (talk) 17:56, 26 April 2017 (UTC)

• Oppose. Similar to my argument for Parkinson's disease, Alzheimer's disease is the more commonly used phrase. Both Harrison's Principle's of Internal Medicine (19th edition) and Kumar & Clark's Clinical Medicine (8th edition) describe Alzheimer's disease. " "Everybody" says "Down's syndrome"." – JeanOhm. It is unclear to me as to why you put "Everybody" in inverted commas. Perhaps you are implying that actually nobody says "Down's syndrome"? To say "Down's syndrome" would require a pause between the two "s" sounds (a glottal stop?), but no-one does that. Rather it is pronounced as a run-on phrase: "Downsyndrome". I suspect that the lack of glottal stop during pronunciation is the main reason why eponymous syndromes tend to avoid the possessive apostrophe & s now. Axl ¤ [Talk] 12:33, 27 April 2017 (UTC)

"maybe this is a more convincing argument. The List of eponymously named diseases, which you led me too, lists alz without the possessive." – JeanOhm. lol, a list article in Wikipedia is not evidence at all. Axl ¤ [Talk] 12:35, 27 April 2017 (UTC)

Rename "Entertainment" to "Media"

Alzheimer's is not entertaining. The section which discusses how Alzheimer's is portrayed in media should be renamed to Media. — Preceding unsigned comment added by Kae verens (talk • contribs) 10:22, 30 April 2017 (UTC)

@Kae verens: You are absolutely correct. I've changed it. Considering how difficult it is to get editors to agree on things, I expect somebody will revert it. JeanOhm (talk) 23:38, 30 April 2017 (UTC)

Semi-protected edit request on 8 May 2017 - "other hypothesis"

Dear editors of this semi-protected page. Please look at the ability to merge/add into the "Other Hypothesis" section of this article. This was the suggestion by reviewer that the hypothesis be added/merged to this page. As the page is semi protected I am using this because it seems reasonable. Please add into the "Other Hypothesis" section of the article.

I am new to editing in wikipedia, and if there is a different way for me to go about this, please simply tell me. I went into the chat/live chat section of wikipedia help and this is the instructions that that suggested for me related to this updated information. thank you. Gabehall hall (talk) 18:05, 8 May 2017 (UTC)

{{AFC submission|d|mergeto|Alzheimer's disease#Cause|u=Gabehall hall|ns=118|decliner=Yash!|declinets=20170507114628|ts=20170419130015}}

The micron stroke hypothesis is a scientific hypothesis that describes the effects of 8-10 $\mu$m size strokes as the cause of brain damage, dementia, and Alzheimer's disease. This hypothesis concentrates on treatable medical diseases and physiologic disturbances as the etiology of Alzheimer's disease. Description of the medical disorders that need to be accurately evaluated and treated include baseline brain tissue, atrial fibrillation, hypercoaguable state, LDL cholesterol, carotid artery stenosis, tobacco exposure, hypertension, diabetes mellitis, systemic inflammation, and sleep apnea. The hypothesis explains how the smallest vascular insults to the brain may go unnoticed by the individual and unseen on an MRI.

Other research groups have published scientific papers referencing the micron stroke hypothesis.,,

The concepts of the micron stroke hypothesis include a complete and accurate evaluation of a unique patient. Following the process has resulted in a case of reversal of Alzheimer's disease.

References

-- Gabehall hall (talk) 18:05, 8 May 2017 (UTC)

Medical hypothesis is generally not accepted as a source. Please see WP:MEDRS Best Doc James (talk · contribs · email) 04:31, 9 May 2017 (UTC)

Journal of Medical Hypothesis come up as a peer reviewed Elsevier journal. "normally in current journal articles that are not in accordance with the main paradigm of the medical society cannot be accepted". I read the micron stroke hypothesis and its to s better than any other listed. Journal of Med hypothesis isnt on controversial Baells list. its a peer reviewed with editorial board - thats not a primary source? also the micron stroke hypothesis comes right up on pubMed and was indexed in Medline. So i am curious as to the other criteria preventing information use. (given the total lack of real advancement in dementia treatment i follow this pageclose). other thoughts? Organicbean (talk) 22:02, 10 May 2017 (UTC)

Details here Wikipedia:Identifying_reliable_sources_(medicine)#Biomedical_journals Doc James (talk · contribs · email) 00:14, 11 May 2017 (UTC)

As of now we have:

A neurovascular hypothesis has been proposed which states that poor functioning of the blood–brain barrier may be involved.

There are a number of newer review sources that should update and expand upon this statement, to the general idea that any of TBI, hypertension leading to small vessel disease, microinfarcts, or inflammation can lead to blood in the grey matter, and that this in turn triggers an AD process. Essentially this implies that the distinction between vascular dementia and AD is less clear than had been thought, and that difficulty in detecting microbleeds corresponds to difficulty in confirming the association. Have a look at PMID 22338577, PMID 23980072, PMID 25510382, PMID 28210211, PMID 24614908, PMID 21778438 (and the comment on the last at PMID 21940969). I'm sure there's a sensible sentence or two that could be crafted from all that. LeadSongDog come howl! 20:29, 11 May 2017 (UTC)

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Vision

Certain aspects of this article are beginning to creak with age. The only reference to clinical features relating to vision is from 1999, and the word 'vision' does not appear at all. Meanwhile much research along the whole visual pathway from retina to frontal cortex has revealed striking changes with visual cognitive impairment. This is not surprising since vision comprises so much of the brain. Egocentric inference changes. Color vision is affected. Visual field changes occur. Spatial frequency sensitivities change. Motion and depth vision changes. This is all long before visual agnosia occurs. Newer tests reflect some of these changes. e.g. All this suggests some serious re-editing of the article. Imersion (talk) 14:46, 17 April 2017 (UTC)

Old discussions

At what point are the discussions in this section deleted or moved to an archive? I was following an interesting aspect of the data that is published here and now that data is gone. Where does it go to? simply deleted? The reason I ask is is that there is much on this page that is not exactly accurate and updates for those affected by this disorder are needed. Vegaproc (talk) 17:23, 16 June 2017 (UTC)

Discussions that are stale for more than 30 days will be archived. There's a search box at the top of the page where you can search all the talk page archives related to this article. Or, just look up the specific discussion you are looking for in this index. -- ChamithN (talk) 17:31, 16 June 2017 (UTC)

If you could point out what aspects you understand are not exactly accurate and WP:MEDRS sources supporting the lack of accuracy that would be useful. Jytdog (talk) 20:06, 16 June 2017 (UTC)

Eponymous medical terms

Hi -- I think this disease should be called "Alzheimer disease", not "Alzheimer's disease". This is consistent with the AMA manual of style, Stedman's dictionary, and Dorland's dictionary. — Preceding unsigned comment added by Drewbaldwin (talk • contribs) 14:24, 18 June 2017 (UTC)

The problem is that in the relevant medical literature it is called "Alzheimer's disease". (See references section of the article.) Ruslik_Zero 18:21, 18 June 2017 (UTC)

See also Talk:Alzheimer's_disease/Archive_12#Move_request.-gadfium 02:18, 19 June 2017 (UTC)

Also, to counter your point, Oxford Dictionary of English calls it 'Alzheimer's Disease' or simply 'Alzheimer's', as the disease is named after a person and not actually a specially coined term for this neurodegenerative disease. [sk9c00] 121.33.145.22 (talk) 21:39, 23 June 2017 (UTC)

Type 3 Diabetes as a Semi-Definite Cause Hypothesis/Theory

Recent studies (de la Monte, 2012) and literature reviews (Kandimalla et al., 2016, ) have pretty strong evidence that supports that at least all sporadic Alzheimer's is caused by or at least can be called Type 3 Diabetes Mellitus, i.e 'localised' brain insulin & IGF-1 resistance leading the cascade of AD pathogenesis. this study also suggests that "...insulin resistance in tissues outside the brain with or without hyperglycemia can potentially cause insulin resistance in the brain and thereby contribute to the onset of Alzheimer's disease.".

References

[sk9c00] 121.33.145.22 (talk) 21:39, 23 June 2017 (UTC)

This is not a review[6]

This [7] could be sufficient to mention the idea in the research section. Doc James (talk · contribs · email) 23:05, 23 June 2017 (UTC)

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• Added archive https://web.archive.org/web/20080223082753/http://www.helpguide.org/elder/alzheimers_behavior_problems.htm to http://www.helpguide.org/elder/alzheimers_behavior_problems.htm

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Plasmalogen

Hi guys. I think it is meaningful to describe the association of the disease with plasmalogens. In addition to the accumulating biochemical data, it has recently been shown that oral administration of plasmalogens could be benificial to mild Alzheimer's disease patients.

References

--— Preceding unsigned comment added by Tetsuotsukamoto (talk • contribs) 14:09, 19 July 2017 (UTC)

Thanks for posting. The Plasmalogen article needed much better sources, and I fixed that. The new ref about the clinical trial is a recent primary source, and we wait for it to be discussed in reviews per WP:MEDREV. Will keep an eye out for that! Jytdog (talk) 23:55, 19 July 2017 (UTC)

Semi-protected edit request on 2 September 2017

The professor in Still Alice teaches at Columbia and not Harvard. 71.218.22.79 (talk) 05:46, 2 September 2017 (UTC)

Corrected, thanks. --Zefr (talk) 05:52, 2 September 2017 (UTC)

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Change of word

In the heading Management - Medications. Term "useful" referring to glutamate should be changed to: "Glutamate is the major excitatory neurotransmitter of the nervous system."

Edited. Thanks. --Zefr (talk) 15:47, 29 September 2017 (UTC)

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Another typical symptom not mentioned here

... is the patient's absolute insistence on erroneous facts. You can assure them over and over that they are incorrect, but they will stick with their fixed idea, e.g. that they have no children, or that you live in Saskatchewan. You may correct them, but 10 seconds later they repeat the wrong facts.--dunnhaupt (talk) 21:53, 12 October 2017 (UTC)

Suggested content

How do you feel about adding this to the bottom of the Diagnosis section?

Due to low accuracy, the C-PIB-PET scan is not recommended to be used as an early diagnostic tool or for predicting the development of Alzheimer's disease when people show signs of mild cognitive impairment (MCI). The use of ¹⁸F-FDG PET scans, as a single test, to identify people who may develop Alzheimer's disease is also not supported by evidence.

I welcome any suggestions that you may have. Thanks, Jenny JenOttawa (talk) 02:18, 13 October 2017 (UTC)

Looks great to me :-) Doc James (talk · [[

Thanks, I appreciate the feedback. JenOttawa (talk) 11:59, 17 October 2017 (UTC)

References

I added some info about Alzheimer's Disease that was discovered in Dolphins

A study was published yesterday about this. I added some brief information about it to the lede. The study also suggests that it may be a cost of a longer lifespan. I was hesitant to add this because this article is semi-protected. Is this an acceptable addition? Xanikk999 (talk)

Does not belong in the lead. Maybe in the research section. Doc James (talk · contribs · email) 19:48, 24 October 2017 (UTC)

This is a review of animal studies which leads the authors to hypothesize about the relationship of longevity - seen in humans and dolphins - to Alzheimer's and diabetes onset, abstract here PMID 28972881. It is primary research, speculative, and not consistent with the article's sections on causes, pathophysiology, or research. --Zefr (talk) 19:56, 24 October 2017 (UTC)

Can I include this in the article?

I made an edit before either to this article or the article on Dementia about research and it was reverted. So I am asking beforehand whether it would be worthy to include new information I found. Apparently the second phase three clinical study of a drug called LMTX was published today. It suggests the drug may slow the rate of atrophy of brain tissue in patients with Alzheimers. Xanikk999 (talk) 22:15, 29 November 2017 (UTC) Source: https://medicalxpress.com/news/2017-11-phase-results-lmtx-published.html Xanikk999 (talk) 22:15, 29 November 2017 (UTC)

Xanikk999: For an encyclopedia, we provide conclusions and facts based on systematic reviews, multiple clinical trials having the same result, or consensus from expert clinical organizations; see WP:MEDSCI. An ongoing or concluded Ph. III clinical trial is not final and the drug may fail in the approval process. It is news and "suggests" something that is not a conclusion; WP:NOTNEWS, WP:CRYSTAL. Thanks for inquiring here first. Fyi, a tutorial on medical editing. --Zefr (talk) 23:21, 29 November 2017 (UTC)

Neuroenergetic Hypothesis

A new paper appears in the November 7, 2017 issue of the Journal of Alzheimer's Disease. Neuroenergetic Hypothesis: Paper Its contents and implications need to be addded to the discussion regarding AD. Much falls into place when the pathogenesis of AD is viewed from a neuroenergetic perspective.

Persuasive has been evidence that: 1. Energy status influences enzyme kinetics and helps determine whether the Amyloid β protein precursor is acted upon by α-secretase – which leads to the production of soluble peptides that readily cross the blood-brain barrier, OR β-secretase – which leads to the production of the less soluble amyloid β that does not readily cross the BBB. 2. Amyoid-β has antimicrobial qualities. This suggests that the shift to favor its production in an energy-deficient CNS (amidst sufficient energy elsewhere in the body) is likely to be a defensive mechanism. The accompanying inflammation, reported with AD, supports the logic of this interpretation. 3. The APOe4 genetic trait (in the animal model) is associated with a decreased (29% in the mouse) ability of glucose to cross the blood-brain barrier. Having a genetically-reduced baseline trait would explain the earlier age of onset in those who carry two copies of this gene. 4. Ample corroborating evidence from animal models as well as biochemical, clinical, epidemiological and pathophysiological sources.

There is also an important message regarding food and lifestyle. A healthful, plant-based, whole foods diet, along with an active lifestyle, lowers the risk of a variety of diseases including those involving the vascular system, diabetes, hypertension, obesity, and heart disease. Both healthful diets and lifestyles have long been associated with a lower risk of AD. The neuroenergetic hypothesis now provides a plausible rationale for adding AD to the list.

Tests are available that can be retooled to track the ability of glucose to cross the BBB and identify at what point in life the energy resources for the brain become inadequate. These tests can reveal when we have gone past that energy turning point – which would be well before AD has a chance to get established. From that point on, steps can be taken to assure that the brain has the energy it requires. This could involve dietary, lifestyle, and pharmaceutical interventions, including alternate (non-glucose) sources of energy the brain can use when not enough glucose is available. We may have to identify a new “conditionally essential” nutrient – a source of metabolizable energy for the CNS – that becomes essential once the amount crossing the BBB is insufficient for normal CNS functionality.

My thoughts are that there is a limited likelihood to “cure” Alzheimer’s disease, but what is exciting is that the process that leads to AD may be identified early in life and prevented well before it can impact cognition. The current therapeutic approach, dealing with treating symptoms in those already diagnosed, is tantamount to attempts to prevent a tub from overflowing but ignoring the fact that faucet remains on. It has proven disappointing, helping to explain why Alzheimer's disease remains the only disease in the top 10 cause of death for which there are no effective treatments or definitive methods for prevention.

As author of the paper I would be willing to write or work with any individual interested in integrating these concepts into the AD piece.Blonz (talk) 00:58, 30 November 2017 (UTC)

Congratulations on the publication of your article. However, any report with the word "hypothesis" in it can't meet the consensus for evidence and source standards of WP:MEDRS. Shortening the message subhead. See the MEDRS tutorial offered here. --Zefr (talk) 01:11, 30 November 2017 (UTC)

NB: I moved this to the bottom where new comments go. Zefr's comment now refers to the section above. I second the comment. A brief summary of this paper could at Alzheimer's_disease_research#Insulin_sensitizers_and_Intranasal_insulin however. There is another review there about intransal insulin (which has been in clinical trials), and is based on this "diabetes type III" notion. Axona was marketed as a medical food based on this hypothesis as well. Jytdog (talk) 05:13, 30 November 2017 (UTC)

It should be appreciated that most concepts are hypothetical regarding the etiology of Alzheimer's disease. This paper connects-the-dots and provides a metabolic explanation of its origins that meshes accurately with its expression; a first look, albeit hypothetical, inside the black box of this disease. Data will be coming out from very large epidemiological studies that provide additional support, but even these do not provide the ideal "cause-and-effect" data. As with many other pathologies that take many years to develop, there comes a times to embrace the evidence we have, particular if it is consistent with what we know. I will look at the Alzheimer's disease research area. My interests are to have these concepts considered in the discussion. Blonz (talk) 20:21, 5 December 2017 (UTC)

Your interests are indeed very clear. Please see your talk page. Jytdog (talk) 20:26, 5 December 2017 (UTC)

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"Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer’s disease"

Just posting this so others can add, if suitable.

nature: genetics "Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer’s disease"

https://www.nature.com/articles/ng.3916

Phantom in ca (talk) 16:57, 18 February 2018 (UTC)

Semi-protected edit request on 7 March 2018

Researchers at the Royal College of Surgeons in Ireland say they have developed a new blood test for early stage Alzheimer's disease. The test analyses the changes in concentration of a small molecule called microRNA in the blood and can enable diagnosis even when symptoms are mild. It is also capable of distinguishing Alzheimer's from other brain diseases with similar symptoms and of predicting how the disease will develop. The research is being carried out by scientists and clinicians from Ireland and Spain. Corkmans (talk) 12:32, 7 March 2018 (UTC) Corkmans (talk) 12:32, 7 March 2018 (UTC)

References

 Not done: although promising, this is more news (WP:NOTNEWS), and does not meet WP:MEDSCI. --Zefr (talk) 14:17, 7 March 2018 (UTC)

WIAFA

Something is out of whack here. WP:WIAFA:

• 2b. appropriate structure: a substantial but not overwhelming system of hierarchical section headings

There are numerous short, choppy sections, and the TOC is overwhelming. The problems are most obvious in "Research directions", where there is mention of clinical trials in 2008 and one-sentence sections :/ SandyGeorgia (Talk) 01:20, 10 April 2018 (UTC)

And this will mean a major update is needed here. SandyGeorgia (Talk) 18:18, 10 April 2018 (UTC)

That so-called "new definition" isn't new at all. Axl ¤ [Talk] 12:00, 18 April 2018 (UTC)

How is it that hippocampus is never mentioned in this article? SandyGeorgia (Talk) 17:52, 14 April 2018 (UTC)

The bulk of the refs predate 2009, so an update is clearly in order. Many could be trimmed in the process. Better antemortem biomarkers are now available, at least in advanced centres. Most of the prevention and treatment trials that were underway then have either failed or been inconclusive, but the better tools should mean a faster pace for future trials. We likely should have better discussion of the BBB microbleeds as seen in sub-mm imaging and of the cascade hypothesis. LeadSongDog come howl! 18:41, 19 April 2018 (UTC)

new research re. HHV-6A and HHV-7 and AD

Herpes viruses are thought to interfere with the the limbic system, which plays a key role in our emotions, moods and instincts.

But until now, this was just a theory to explain associations seen between blood samples and Alzheimer's disease development.

In the new research, the authors found not only that Alzheimer's patients not only had higher levels of two strains of the herpes virus - HHV-6A and 7 - but that these viral genes were actively disrupting the human genes that increase Alzheimer's risks.

'What's clear is that they're perturbing networks and participating in networks that directly accelerate the brain towards the Alzheimer's topology,' says Dr Dudley.

These two viruses are not sexually transmitted, like the previously studied HSV-1.

Rather, HHV-6A and 7 are extremely common viruses that 90 percent of children pick up in their first few years of life and they often remain asymptomatic.

'We found viral genes in the brains of our patients with Alzheimer's to much greater extent as compared to aged controls and patients with other neurodegenerative diseases,' study co-author Dr Sam Gandy told Daily Mail Online.

From: http://www.dailymail.co.uk/health/article-5870075/Herpes-strains-90-percent-abundant-brains-sufferers-study-finds.html

Someone should review the original study and, if appropriate, add its information or just a citation to it. Phantom in ca (talk) 20:53, 21 June 2018 (UTC)

We don't care what the daily mail says here per WP:DAILYMAIL and we don't cite primary sources (the actual study. Please see WP:MEDRS. Jytdog (talk) 20:56, 21 June 2018 (UTC)

I agree that the Daily Mail is not a usable source, and that the paper is a primary source. However, it was published in Neuron ( https://www.cell.com/neuron/fulltext/S0896-6273(18)30421-5 ), one of the top neuroscience journals, and has received coverage by much stronger sources. We still shouldn't include it here until it receives coverage from proper secondary sources, but it is something to keep an eye on, and doesn't deserve being closed down with extreme prejudice. Looie496 (talk) 22:29, 21 June 2018 (UTC)

LOL at Jytdog who apparently is either trying to start a fight or didn't read my entire post ("Someone should review the original study and, if appropriate, add its information or just a citation to it.") Thanks Looie496 for linking to the original. Phantom in ca (talk) 00:23, 22 June 2018 (UTC)

The terms "Senile" and "Senility"

The discussion at Talk:Dementia#Senile_/_Senility may interest watchers of this talk page. PamD 21:16, 6 August 2018 (UTC)

Is Metabolic syndrome a risk factor for cognitive impairment and Alzheimer

Is Metabolic syndrome a risk factor for cognitive impairment and Alzheimer? Tadeu.gross (talk) 15:58, 13 August 2018 (UTC)

Methylphenidate for the treatment of apathy in patients with Alzheimer Disease

A recent review found that methylphenidate may be useful in improving apathy, a common condition, in patients with Alzheimer Disease. The evidence discovered in this review is of low quality, however, and more high-quality research should be conducted to confirm methylphenidate as an appropriate pharmacotherapy for apathy.Mcbrarian (talk) 13:50, 18 September 2018 (UTC)

It's difficult to find consensus on how we might approach improving apathy among patients diagnosed with AD. The two recent reviews cited here reference low-quality studies as an indication that higher quality research needs to be conducted in this field. I think it's important to include a statement about apathy management. Apathy is mentioned periodically throughout this article, but I do not see a discussion on how it may be managed. — Preceding unsigned comment added by Mcbrarian (talk • contribs) 13:57, 18 September 2018 (UTC)

Almost all research reviews call for more research, that's not really instructive. If the recent reviews disagree with each other, we can simply state what they found. If the reviews agree that the primary findings are inconclusive, we can state that. But Wikipedia cannot engage in wp:SYN, even based on reviews. There are lots of other places to publish original research, but not here. LeadSongDog come howl! 14:43, 18 September 2018 (UTC)

user:LeadSongDog Sorry - I wasn't claiming that we need to synthesize the findings from these two articles. In fact, only the first explicitly reviews studies of Methylphenidate. The second is a related study that includes Methylphenidate as well as other interventions for apathy in patients with Alzheimer's. The second review I cited found the same outcomes as the first with respect to Methylphenidate. I wouldn't call that synthesis, would you? A solution might be to only cite the first review. What do you think? Mcbrarian (talk) 15:00, 18 September 2018 (UTC)

Cochrane reviews are normally the best we can hope for, but in this particular case, the review is, to my mind, rather problematic. Looking at who the Cochrane reviewers are, then look at how often they cite themselves in the review, particularly in the discussion of methylphenidate for apathy. The Theleritis & alia review does not exhibit this problem and (as you say) it more or less agrees on the basic point, one saying: "Stimulants like methylphenidate alone or in combination with AChEIs have been also proven beneficial" while the other says:"From the three trials with methylphenidate, we found that it may improve apathy, although this depended on how the apathy was measured. The people taking methylphenidate also did slightly better than those taking placebo on scales measuring cognition (thinking, remembering, etc.) and some daily activities, but it was not clear that these effects were big enough to be important in practice." So they assessed the evidence and effect as weaker but having the same tendency as Theleritis. Please have some other WPMed editors look at the question, but I would suggest something along the lines of: "In small studies methylphenidate has been found to improve apathy slightly"(citing both).LeadSongDog come howl! 21:11, 18 September 2018 (UTC)

One could summarize the Cochrane review as "There is tentative evidence that methylphenidate improves apathy and may have a small amount of benefits for cognition in people with AD." Hardly a strong endorsement. Doc James (talk · contribs · email) 06:56, 19 September 2018 (UTC)

I would lean towards excluding it. The evidence is too weak to include it. But if we are including it then Doc James’ suggested text looks a reasonable summary of the source.--Literaturegeek | T@1k? 10:38, 19 September 2018 (UTC)

Although reviews, both papers summarize low-quality research on relatively small numbers of subjects, with admission in the abstracts that results are too preliminary to apply in clinical practice, i.e., not suitable for an encyclopedia, except possibly in the Research section. Related review PMID 28960446. --Zefr (talk) 00:17, 1 November 2018 (UTC)

References

new research showing CNS HSV1 associated w/AD

It follows up on the researchers' previous studies. Article -- by Ruth Itzhaki is Professor Emeritus of Molecular Neurobiology at University of Manchester -- with plenty of embedded links to original studies here: http://www.bbc.com/future/story/20181022-there-is-mounting-evidence-that-herpes-leads-to-alzheimers Just a FYI in case it calls for an update to this Wiki article. Phantom in ca (talk) 23:37, 31 October 2018 (UTC)

Another popular article about different researchers into the HSV infection hypothesis, also w/embedded links to :studies: https://www.statnews.com/2018/10/29/alzheimers-research-outsider-bucked-prevailing-theory/ Phantom in ca (talk) 05:09, 1 November 2018 (UTC)

Semi-protected edit request on 4 November 2018

Evolution

Evolutionary Hypotheses

There are several hypotheses regarding the evolutionary origin of Alzheimer’s disease. The first of these hypotheses is that the disease is the inevitable occurrence of senescence in the human brain occurring due to accumulation of ancient inflammatory proteins or adaptive metabolic reduction . The second of these hypotheses is that the rapid growth and robust neuroplasticity in the human brain that occurs especially during the developmental and reproductive years and has been evolutionarily favored comes with the cost of higher risk of brain damage later in life

I am proposing to add a section regarding the evolution of the Alzheimer's describing the evolutionary hypotheses regarding the origins of the disease. Amoghnarendra (talk) 05:00, 4 November 2018 (UTC)

 Not done: please establish a consensus for this alteration before using the {{edit semi-protected}} template. Given that this edit is the addition of an entire section, consensus should be sought. If this was an uncontroversial edit, like fixing typos, adding references, or correcting inaccuracies, this would have been okay. Feel free to ask me any questions on my talk page. DannyS712 (talk) 23:00, 4 November 2018 (UTC)

Semi-protected edit request on 1 December 2018

Evolution ===

Evolutionary Hypotheses ====

There are several hypotheses regarding the evolutionary origin of Alzheimer’s disease. The first of these hypotheses is that the disease is the inevitable occurrence of senescence in the human brain occurring due to accumulation of ancient inflammatory proteins or adaptive metabolic reduction . The second of these hypotheses is that the rapid growth and robust neuroplasticity in the human brain that occurs especially during the developmental and reproductive years and has been evolutionarily favored comes with the cost of higher risk of brain damage later in life

One plausible evolutionary process is that the formation of plaques are a mechanism of an ancient inflammatory process in the immune systems of jawed vertebrates. Plaques have been revealed to contain other ancient inflammatory proteins besides amyloid that played a role in wound healing and inflammatory processes, such as pentraxin, which is highly conserved in mammals. Amyloid beta has been shown to act as an antimicrobial peptide even inhibiting the growth of strains of streptococcus bacteria, E. coli, etc. Thus, the pathology of Alzheimer’s disease may be caused by a process that evolved to protect the brain, but is acting improperly and doing damage.

Adaptive metabolic reduction theory posits that a decrease in human brain activity is associated with adaptive programs that decreased the energy requirements for hunter-gatherers who could not afford the significant metabolic toll of the brain at the 30s, 40s, and 50s with an inconsistent diet. The aging foragers would not have required the same cognitive capacities as younger foragers due to accumulated cognitive learning. The clinical effects of AD would not have occurred in these foragers due to shorter lifespans and thus there would not exist any selective pressure against the maladaptive effect of the adaptive programs. Metabolic reduction theory is also linked to the thrifty gene hypothesis which is linked to the development of insulin resistance or diabetes and increased fat composition.

Studies in mice have demonstrated that increases in synaptic activity also results in an increase amyloid plaques which lead to the production of plaques as mice age. Genes involved in synaptic plasticity that promote neuroplasticity and larger brain sizes have also been shown to be involved in Alzheimer’s disease. One such gene is the Ε4 allele of the ApoE gene. This gene has a higher rate of synaptic activity compared to the norm corresponding to a higher risk of Alzheimer’s. The E4 allele of the ApoE gene mentioned in the previous study has been shown to have a high prevalence in the population (28% of humans carry one copy) even with its correlation to the Alzheimer’s pathology. ApoE E4 is believed to continue to persist in the population as the selective pressure against ApoE E4 decreases with age. It has also been suggested that this allele continues to persist in our population as the other variants of the ApoE gene such as ApoE E2 increase the risk of atherosclerotic disease while the ApoE E4 gene may protect against liver damage, reduce cardiovascular response to mental stress, etc. ApoE E4 is expected to be eliminated from the population with the rise of the cognitive protective alleles, ApoE E2 and E3.

Alzheimer’s disease in the Animal Kingdom====

In the animal kingdom, apes have a buildup of amyloid plaque similar to what is found in humans with Alzheimer’s disease pathology but notably do not suffer from the same symptoms as humans. Other members of the animal kingdom such as the ungulates, cetaceans, elephants, marsupials, birds, reptiles, amphibians, and fish contain some or no features of the Alzheimer’s disease pathology but do not suffer from any symptoms of Alzheimer’s disease present in humans suggesting that apes would serve as the best model species to analyze how differences in brain development and function brought upon Alzheimer’s in humans. Chimpanzees possess an amyloid precursor protein and tau protein identical to humans indicating that the amyloid plaque buildup is structurally similar to humans as well. In addition, apes with this pathology do not see the loss in neuronal density seen in humans indicating that Alzheimer’s is unique to the human genotype. A comprehensive study of 20 brains from older chimpanzees revealed that the amyloid plaque buildup and tau tangles was occurring in 12 of these chimpanzees, but the study did not conclusively contradict claims that chimpanzees do not have cognitive declines due to plaques and tangles. Until Alzheimer’s disease is identified in other animal species, it can be classified as a uniquely human disease.

Evolutionary Medicine====

The hypothesis that amyloid-beta plaques are evolutionary holdovers of an ancient inflammatory system and evolved to protect the brain from damage may require that treatments such as anti-amyloid beta immunotherapy be examined to ensure that there is a clear net benefit to these treatments. A trial of AN1792, an experimental anti-amyloid beta agent, demonstrated significant declines in amyloid beta plaques but no reversal of symptoms of dementia pointing to the theory that the plaques may be a protective agent ensuring brain homeostasis. Another set of trials for a gamma-secretase inhibitor that prevents amyloid-beta plaque formation were prematurely ended when it was discovered that the treatment was exacerbating brain deterioration in comparison to the placebo treatment. The potential evolutionary origins of Alzheimer’s disease pose questions to current treatments of the disease involving treatment of amyloid-beta plaques and tau tangle pathology which may serve as a source of resistance to cognitive decline in certain brains and an exacerbation in other brains.

References

Amoghnarendra (talk) 04:59, 1 December 2018 (UTC)

 Not done: it's not clear what changes you want to be made. Please mention the specific changes in a "change X to Y" format and provide a reliable source if appropriate. DannyS712 (talk) 06:49, 1 December 2018 (UTC)

I would like to add an evolution section to the Alzheimer’s disease wikipedia page describing the evolutionary origins of the rising amount of neurodegenerative diseases around the world. The Wikipedia page on Alzheimer’s disease does not currently cover the current theories on the evolution of Alzheimer’s disease in terms of the perspectives of natural selection, adaptation, genetic drift, etc. This topic is of extreme importance to medicine — Preceding unsigned comment added by Amoghnarendra (talk • contribs) 21:52, 1 December 2018 (UTC)

Hi Amoghnarendra. Thanks for wanting to improve the article. There are a few issues here.

1) What we do here in Wikipedia, is summarize reliable sources. Every word that you write, needs to be summarizing a source -- there can be none of your own thinking or analysis in the content (See the No original reserarch policy). There is a bunch of your own thinking in the content above.

2) The kinds of sources that are reliable for content about health, are defined in WP:MEDRS - the kinds of sources we look for are recent literature reviews in high quality journals, and statements by major medical and scientific bodies. Textbooks are OK too. You have a bunch of old sources, and primary source as well (e.g the chimpanzee study).

3) This stuff should really be in Alzheimer's disease research, not here on the main page about the disease. Jytdog (talk) 22:07, 1 December 2018 (UTC)

Diagnosis : Techniques

Under Diagnosis you have a section called Techniques. This makes sense as part of Diagnosis Techniques, but would be better as Diagnostic Tests.Imersion (talk) 12:21, 11 December 2018 (UTC)

Thanks for the idea. For deciding on headings we usually try to follow WP:MEDMOS. I am not certain how subheadings are determined. @Doc James: do you have any more feedback on determining subheadings for @Imersion:? Thanks! JenOttawa (talk) 02:45, 12 December 2018 (UTC)

Not based on a single test but a process. I think techniques is fine. Also we do not capatalize every word in a heading. Doc James (talk · contribs · email) 09:27, 12 December 2018 (UTC)

Management : Multifactor

This study shows promise for reducing symptoms: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4221920/ — Preceding unsigned comment added by FeasibleAlternative (talk • contribs) 19:43, 25 December 2018 (UTC)

Introductory text: "4 5%" instead of "4 to 5%" for early onset AD figure

In the last paragraph of the introduction, there is a mistyped figure, stating "4 5%" instead of "4 to 5%" (or "4-5%") regarding the percentage of early onset Alzheimer disease compared to late onset. It is quite important IMHO as it could raise extra stress in readers, if they would understand "45%" (which is completely wrong) instead of "4 to 5%" of early onset AD.

How to fix it: Sentence: "It most often begins in people over 65 years of age, although 4 5% of cases are early-onset Alzheimer's" ...Should read "It most often begins in people over 65 years of age, although 4 to 5% of cases are early-onset Alzheimer's"

The true figure can be checked easily in the reference given within the page (ie. reference "[3]": Mendez MF (November 2012). "Early-onset Alzheimer's disease: nonamnestic subtypes and type 2 AD". Archives of Medical Research. 43 (8): 677–85. doi:10.1016/j.arcmed.2012.11.009. PMC 3532551. PMID 23178565.)

Nekonaute (talk) 09:45, 18 February 2019 (UTC)

 Done (Special:Diff/883946865). I believe that in cases like these, en dashes are preferred over "to", so I've slightly modified your suggestion accordingly (anyone feel free to correct me if I'm wrong about that). Thanks for catching that Nekonaute, that's definitely an important typo to fix!--SkyGazer 512 ^{Oh no, what did I do this time?} 16:50, 18 February 2019 (UTC)

Animated GIF of smoothened cortex is misleading

There is cortical atrophy in Alzheimer's disease affecting much of the cerebral hemispheres and hippocampus.

In Alzheimer's Disease, the cortex typically shrinks so there is increased space between gyri. This image instead shows a filling up of sulci and smoothening of cortex. The source of the image is rather dubious. I suggest deleting it.Thinksthanks (talk) 23:12, 18 February 2019 (UTC)

I agree! It does not adequately represent the evolution of Alzheimer's and is even misleading in terms of anatomopathology. Spyder212 (talk) 03:16, 19 February 2019 (UTC)

OK, I tried to remove the image but the page is protected so I'll leave that to someone else. I suggest removing the image from Wikipedia entirely, not just from this article.Thinksthanks (talk) 18:30, 19 February 2019 (UTC)

Hi, this discussion made sense, so I am removing the image. DrJanaOfficial (talk) 10:59, 07 Marh 2019 (UTC)

Yah looking at it more closely agree. Doc James (talk · contribs · email) 11:57, 7 March 2019 (UTC)

Alzheimer’s Disease is a ‘Double-Prion Disorder,’ Study Shows

https://www.ucsf.edu/news/2019/05/414326/alzheimers-disease-double-prion-disorder-study-shows

Leaving this here since I don't know what to make of it. 173.228.123.207 (talk) 21:34, 1 May 2019 (UTC)

Cause

I don't see Porphyromonas gingivalis mentioned as a possible cause for the disease. See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6357742/ Perhaps mention it in article ? Genetics4good (talk) 06:33, 14 May 2019 (UTC)

Semi-protected edit request on 19 June 2019

Correct "Behavioural" to "behavioral." Correct "characterised" to "characterized." Correct "regognise" to "recognize." Correct "critisised" to "criticizedVinGraves (talk) 02:44, 19 June 2019 (UTC)." VinGraves (talk) 02:44, 19 June 2019 (UTC)

 Not done: please establish a consensus for this alteration before using the {{edit semi-protected}} template. This article is written British English - FlightTime (open channel) 02:47, 19 June 2019 (UTC)

In a long ago job I worked at a state hospital ward that had old men who caught syphilis long before penicillin was discovered. The showed the signs od Alzheimers long before Alzheimers was heard of. It was just called syphilitic dementia. Herpes is now suspected but I suppose any infection or untreated VD will eventually be implicated. Ovarian cancer, , prostate cancer, cervical ........ — Preceding unsigned comment added by 75.68.248.198 (talk) 20:06, 29 June 2019 (UTC)

Semi-protected edit request on 21 July 2019

Suggest adding new text and reference to JAMA paper to reflect recent findings (https://jamanetwork.com/journals/jama/article-abstract/2738355):

Among older adults both an unfavorable lifestyle and high genetic risk are independently associated with higher dementia risk. A favorable lifestyle is associated with a lower dementia risk, regardless of genetic risk. David.j.llewellyn (talk) 16:13, 21 July 2019 (UTC)

Might be good to wait for a review article. Although this study is large it's still a primary source and we generally try not to overemphasize single studies (WP:MEDRS). --80.254.69.69 (talk) 13:53, 27 July 2019 (UTC)

 Not done for now: Echoing what the IP said. We should wait for a review. --Trialpears (talk) 22:23, 13 August 2019 (UTC)

Other hypothesis: amyloid as an in-brain immune system, and AD driven by infections

Dr Dale Bredesen has spoken on Radio New Zealand: https://www.rnz.co.nz/national/programmes/afternoons/audio/201859071/can-alzheimer-s-be-prevented-or-reversed

and received rebuttal which does not seem to go to the factual content of the claims: https://www.rnz.co.nz/national/programmes/afternoons/audio/201859225/alzheimers-nz-responds-to-dr-dale-bredesen

In so far as I find his position comprehensible, it seems to cast amyloid as part of an innate immune system which is specific to the brain, and to recommend resolving the threats that trigger that immune system.

Ideally, someone with expertise in the subject-matter would check this interpretation before it got into the main page. ArthurDent006.5 (talk) 09:02, 5 November 2019 (UTC)

Edit request to update other hypotheses, as retrogenesis has made the list - time to include other published hypotheses

"The increased incidence of AD in patients suffering from hypertension and irregular heartbeat,gave rise to the hypothesis of “micron strokes”. Micro-strokes caused by fibrous eythrocyteemboli or micron-sized cholesterol crystals could act as “seeding points” for the growth of amyloidplaques as a healing response. " REFERENCE: Hamblin, Michael R. "Photobiomodulation for Alzheimer’s Disease: Has the Light Dawned?." Photonics. Vol. 6. No. 3. Multidisciplinary Digital Publishing Institute, 2019.

Rational:Other hypotheses the list currently includes hypotheses related to tobacco, air pollution, oligodendrocyte dysfunction, retrogenesis, neurodevelopment/neuromodulation and celiac disease. This page would be better to also include some hypothesis that have been referenced and written about in the medical literature. Background: in the past this page seemed to be controlled by the "amyloid club" and no other work was ever really added to the "other hypotheses" section without it being taken down in the next review.

Talking point: the amyolid hypotheses is dead - time to move on and stimulate other ways to solve medical problems and wikipedia not having political agenda should be more inclusive of published and referenced medical literature. — Preceding unsigned comment added by Ltk59 (talk • contribs) 16:49, 9 October 2019 (UTC) Ltk59 (talk) 10:51, 22 October 2019 (UTC)

Can you please add a section on the Alzheimer's Disease page about the link with HSV 1? I think it is very pertinent information...

I did not add as a suggestion, but written it would be good to also add some of the info from the HSV 1 'world" also to the other hypothesis section Ltk59 (talk) 10:51, 22 October 2019 (UTC)

First, Ltk59, new talk page comments go to the bottom and requests for a revision should include the proposed text and a strong review. Personally, I feel this section on "Other hypotheses" is guesswork and unencyclopedic with no strong sources and most conclusions about the various onset mechanisms as uncertain and in need of much further research and future reviews. A PubMed search about HSV-1 is here, convincing me that little encyclopedic information is available. Wikipedia is not a journal or textbook about all things from primary research concerning unproven hypotheses, WP:NOTTEXTBOOK #6-7. --Zefr (talk) 15:48, 22 October 2019 (UTC)

There are now (5 November 2019) 51 hits on PubMed, of which about 10 appear to be misdirected. I have no idea how many hits would be required to make a mechanism seem certain. ArthurDent006.5 (talk) 09:11, 5 November 2019 (UTC)

MDPI

Have trimmed as probably predatory.

Have also removed the primary sources. Doc James (talk · contribs · email) 18:57, 27 February 2020 (UTC)

Addition of a relevant Cochrane review

I am considering adding the following review to this page in a relevant section to add content and scope of information. Do any more experienced editors have any suggestions or comments? I have already added this to the page on Mild Cognitive Impairment Thank you BDD user (talk) 15:21, 2 March 2020 (UTC)

References

Although a Cochrane report, that study is preliminary, limited to 45 people in just one study, and inconclusive, with the authors stating "We cannot make any recommendation regarding the routine use of 18F‐florbetaben in clinical practice based on one single study with 45 participants." Because using 18F‐florbetaben with PET is a highly expensive scan, this doesn't seem likely as a useful AD detection screen, and isn't a strong encyclopedia topic at present. I would say we exclude it until more substantial evidence is available. It seems ok for an entry as research in the MCI article. --Zefr (talk) 15:35, 2 March 2020 (UTC)

To be clear, that quotation is from the Cochrane review, not from the study, and it discusses the test as one of exclusion: without amyloid, any dementia is non-Alzheimer's. Still, with N that small, I agree it belongs in research discussions. Alzheimer's disease research would have been the place for it, until it was redirected. LeadSongDog come howl! 17:49, 2 March 2020 (UTC)

Semi-protected edit request on 15 April 2020

I have two edits, both under the "Genetics" header 1. A genome-wide significant loci was also found by Lambert et al 2013 in CD33 2. SLC24A4 is incorrectly written as "SIC24A4" and thus there is no correct link to a further wikipedia page because that gene does not exist.

Please correct. Thank you Ecstage (talk) 14:53, 15 April 2020 (UTC)

@Ecstage:  Partly done: changed SlC24A4 to SLC24A4. GoingBatty (talk) 01:14, 22 April 2020 (UTC)

The work of Dale Bredesen, MD

Dear Editors, I am a person in his 70's, subject to a degree of cognitive impairment, who, on the basis of family history, has been expecting it to develop into Alzheimer's disease.

Recently by chance I came across a book called "An end to Alzheimer's", ISBN-13: 978-1785041228 published in 2017, written by Dale Bredesen MD, a Professor of neurology at the University of California, Los Angeles. He shows that Alzheimer's is not a single disease, there are at least 3 types of cognitive decline, and they can each be slowed or reversed.

This is very important research and I suggest that your page should be saying something about it. But there is a problem: I can not find any secondary sources - e.g the Alzheimer's Association journal says nothing about it. Over to yu Walk Tall Hang Loose (talk) 13:45, 3 May 2020 (UTC)

Semi-protected edit request on 17 May 2020 : Blood Brain Barrier

Recently there has been a very important Nature publication in Alzheimer research:

- paper: https://www.nature.com/articles/s41586-020-2247-3

- nature coverage: https://www.nature.com/articles/d41586-020-01152-8

The paper gives much more credit to the blood brain barrier damage hypothesis in the contest of APOE4 mutation. I think it would be worth it to add a whole paragraph beneath the "causes" or a subparagraph beneath the "genetic causes" as this remarkable paper goes into great depth describing the effect of APOE4 mutation , how the blood brain barrier leaks, how pericite with APOE4 mutation are dysfunctional secreting more cyclophilin A (CypA) and matrix metalloproteinase-9 (MMP9) causing the damage and demise of nearby pericites, and especially how all this is independent of Aβ and tau accumulation.

Suggested change with a paragraph in Causes (sorry i don't know the needed formatting to make it):

Blood brain barrier damage:

A neurovascular hypothesis has been proposed which states that poor functioning of the blood–brain barrier may be involved.[71]. It has been found that the blood–brain barrier (BBB) breakdown may be an early biomarker of human cognitive dysfunction , as individuals with early cognitive dysfunction develop brain capillary damage and BBB breakdown in the hippocampus irrespective of Alzheimer’s Aβ and/or tau biomarker changes. This has been proven in the setting of APOE4 mutated patients where cognitively unimpaired APOE4 carriers already show signs of the breakdown of the BBB in the hippocampus and medial temporal lobe, more severily in those with cognitive impairment, without the fingding being related to amyloid-β or tau pathology. The biomarker of pericyte injury, soluble PDGFRβ ,, in the cerebrospinal fluid predicted future cognitive decline in APOE4 carriers but not in non-carriers. Apparently this damage is driven by dysfunctional APOE4 mutated pericites , which produce more cyclophilin A (CypA) and matrix metalloproteinase-9 (MMP9) causing the damage and demise of nearby pericites. Alessandro313 (talk) 07:16, 17 May 2020 (UTC)

References

@Alessandro313: The authors of the three articles have been doing research on BBB for over five years now. While the results are interesting, they are still only primary sources, and we really would prefer a good secondary source that reviews the field and forms some conclusions about the relative importance of the blood–brain barrier. That would be needed to expand the Causes section. Instead, I suggest that a brief summary in the Research directions - Diagnosis section would be appropriate until secondary sources report on the studies. I've added a sentence and the three sources at the end of the section. --RexxS (talk) 23:34, 4 June 2020 (UTC)

Blood test

It was announced on the BBC Radio Four news this morning (Wednesday 29 July 2020) that a blood test could detect whether people are at risk of Alzheimer's twenty years before they show symptoms. I am sure I heard on the "What the Papers Say" section that the Daily Telegraph talks about this. If any one knows about this and can provide reliable sources, it could be added to the article. This would help Wikipedia to be an up-to-date encyclopedia. 06:15, 29 July 2020 (UTC)

Thanks for the suggestion. If you can find the medical study source and it meets WP:MEDRS (e.g., is it also shared in a high-quality review article or a systematic review) then I can help add this information. Great to have so many people helping to keep the articles up to date! JenOttawa (talk) 16:34, 29 July 2020 (UTC)

MIND Diet-Preventing Alzheimer's

https://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/in-depth/improve-brain-health-with-the-mind-diet/art-20454746 https://health.usnews.com/best-diet/mind-diet

There is still much debate as to how effective diet is in the prevention of Alzheimer's disease, and as well as which diets are the most effective. Further research and clinical study will need to be done, but it seems that the MIND Diet has provided initial results that are promising. It seems that the reason this diet has the potential to be effective in preventing Alzheimer's is because it is rich in foods that are specifically tied to brain health, especially Flavonoids which impact memory. MaloneandStockton (talk) 03:27, 28 September 2020 (UTC)

MaloneandStockton Are you proposing a change or edit to the article, or contributing to a general discussion of the topic of AD and diet? Jaredroach (talk) 17:46, 29 September 2020 (UTC)

Can someone explain to be how diet can stop a sporadic prion disease? 75000cases (talk) 23:08, 8 December 2020 (UTC)

Although Alzheimer shares similar symptoms and brain degeneration to Creutzfeldt–Jakob, the cause is still unknown. There is no direct evidence that it is mediated or caused by prions, and medications which remove the amyloid plaques do not seem to affect the course of the disease. Further, diet literally involves putting things into your body, so it could have an effect even if the disease is caused by a prion infection. For the most obvious example, eating fewer prions would be beneficial. TricksterWolf (talk) 16:52, 29 December 2020 (UTC)

Recent review: inconsistent evidence. [8] SandyGeorgia (Talk) 17:03, 29 December 2020 (UTC)

Please review WP:MEDRS (which Mayo is not). SandyGeorgia (Talk) 01:33, 9 December 2020 (UTC)

The "Stages of Alzheimer disease" infobox is poorly sourced.

I've worked in this area previously. I noticed that "repeats same conversations" is common in early-stage Alzheimer (partial conversations, at the very least), but here it's being described as a late-stage symptom. So I followed the source to see what it says. The source is not a primary source, it's a Consumer Reports article, one which fails to list all of its sources. This is a rather bizarre choice for information about the disease.

Here is a better and more authoritative source for information on the stages of Alzheimer disease:

https://www.alz.org/alzheimers-dementia/stages

I would make changes myself, but I'm uncertain how to properly cite the Association's website and lack the time at the moment to search and learn. TricksterWolf (talk) 16:45, 29 December 2020 (UTC)

We don't cite medical content to advocacy organizations, which are not "authoritative sources" for medical content. (Yes, the article is outdated, see above the need for a Featured article review, but adding advocacy orgs is not the way to correct that. Please review WP:MEDRS.) SandyGeorgia (Talk) 17:04, 29 December 2020 (UTC)

Chronic?

Does the word chronic need to be used since it is defined by neurodegenerative? --Iztwoz (talk) 11:05, 30 December 2020 (UTC)

Went ahead and removed it.--Iztwoz (talk) 15:20, 31 December 2020 (UTC)

smy nana has alzheimer's she changes alot she got angry with dad and i got no idea to stop this alzheimerd — Preceding unsigned comment added by 2001:8003:D062:5400:E437:6A99:A417:DA7C (talk) 04:33, 9 February 2021 (UTC)

Semi-protected edit request on 17 February 2021

Change "can be mistaken for normal age." to "can be mistaken for normal aging." OwenBOSSMan (talk) 07:08, 17 February 2021 (UTC)

 Done Zupotachyon (talk) 07:38, 17 February 2021 (UTC)

Society and Culture

I think it is important to expand upon the health disparities known to be present in the context of Alzheimer's disease. Racial/ethnic identity (e.g., Black, Latinx), for example, is a significant risk factor but is also a sociocultural umbrella term that has been outlined with substantial supporting literature to actually describe the disparities faced by these persons rather than their racial/ethnic identities. --Jcl11 (talk) 21:49, 22 February 2021 (UTC)

Do you have sources? It sounds like there is overlap in the content you suggest between Epidemiology, and Society and culture; which affects whether we need WP:MEDRS sources or just plain WP:RS. It is not clear to me if you are referencing caregiving, prognosis, epidemiology, or which factor ... SandyGeorgia (Talk) 21:54, 22 February 2021 (UTC)

Aluminium

From Alzheimer's disease#Other hypotheses:

The majority of researchers do not support a causal connection with aluminium.

From Immunologic_adjuvant#Humans:

Aluminium salts used in many human vaccines are regarded as safe by Food and Drugs Administration, although there are multiple studies suggesting the role of aluminium, especially injected highly bioavailable antigen-aluminium complexes when used as adjuvant, in Alzheimer's disease development

Shouldn't the statements be synchronized?

References

--Error (talk) 16:06, 12 April 2021 (UTC)

All of the sources, in both articles, are old, and there are numerous newer secondary reviews that should be used. SandyGeorgia (Talk) 16:29, 12 April 2021 (UTC)

confusion on is it genetic or not

The wiki page in summary claims:

"About 70% of the risk is believed to be inherited from a person's parents"

and then in causes in 2.1 under genetics it says:

"Only 1-2% of Alzheimer's cases are inherited"

So this is huge difference. One of the stats are true. Why is summary not aligned with the facts? — Preceding unsigned comment added by Gulabani17 (talk • contribs) 05:12, 14 March 2021 (UTC)

Made some changes with different ref. Thanks --Iztwoz (talk) 13:43, 14 March 2021 (UTC)

Heritability and inherited are two different things. SandyGeorgia (Talk) 13:51, 14 March 2021 (UTC)

Would it be beneficial to define the differences between the two to help the reader understand and not become confused between the two?Ambebeck (talk) 21:55, 3 May 2021 (UTC)

Semi-protected edit request on 11 September 2021

Monoclonal antibodies

A systematic review and meta-analysis concluded that monoclonal antibodies against beta-amyloid induced clinical improvements of small effect sizes and biomarker improvements of large effect sizes. Among individual drugs, aducanumab produced the most favorable effects followed by solanezumab.

Reference https://pubmed.ncbi.nlm.nih.gov/33831607/ 84.205.241.2 (talk) 16:22, 11 September 2021 (UTC)

Not done: it's not clear what changes you want to be made. Please mention the specific changes in a "change X to Y" format and provide a reliable source if appropriate.

Music Therapy

I believe this article could use much more information on research revolving around music therapy. There are only a few sentences that even mention it in the entire article, and even then they seem to quickly dismiss it. Perhaps the information included on music therapy is outdated, which is why it is not mentioned much. There is a large body of current research focusing on the benefits of music therapy to individuals diagnosed with Alzheimer's disease that is worth covering more comprehensively in this article. What do you think about this? --Jrk3110 (talk) 21:31, 29 September 2021 (UTC)

FAR needed

Version reviewed

This is a 2008 Featured article that averages 3,000 daily pageviews whose main writers have not edited since 2012 (OrangeMarlin) and 2013 (Garrondo). It has fallen out of standard and will need to be sent to WP:FAR unless someone takes on the issues, including a comprehensive update. Wherever one glances there are issues:

• The Further reading section contains only dated entries. FAs are supposed to be comprehensive, so items listed there need explanation.
  • Trimmed (t · c) buidhe 21:27, 29 July 2020 (UTC)
• A consistent citation style (the Boghog/Diberri format with vancouver-style authors) has not been maintained.
• The WHO and NIH sources have been considerably used, rather than sourcing to the more authoritative, underlying published literature.
• Many of the sources used are considerably dated-- it does not seem that the article has been routinely updated to newer sources, or is sourced to the highest standards per WP:WIAFA and WP:MEDDATE.
• The Research directions section is particularly problematic, and has become a catch-all (which may work for most articles, but not for the high standards required of a Featured article). That section is using lay sources and has very dated sources as well ... if something in research is significant, it will eventually be mentioned in a secondary review. The Research directions section needs a complete rewrite, using the latest high quality secondary reviews, rather than a catch-all reflecting the popular press.
• The considerable overlap between Dementia with Lewy bodies and Alzheimer's is not developed, with one passing sentence.
• There is a graph of deaths in ... 2012!
• Epidemiology has very dated sources.
• Sourced to 2008! Huperzine A while promising, requires further evidence before its use can be recommended.[189]
  • Removed, no longer promising (t · c) buidhe 21:27, 29 July 2020 (UTC)
• Sourced to 2010! The oldest hypothesis, on which most currently available drug therapies are based, is the cholinergic hypothesis,[52] which proposes that AD is caused by reduced synthesis of the neurotransmitter acetylcholine. The cholinergic hypothesis has not maintained widespread support, largely because medications intended to treat acetylcholine deficiency have not been very effective.[53] Either this hypothesis panned out, or it didn't. If it did, new source. If it didn't, remove, UNDUE. This is similar to what is found throughout the article, which is grossly outdated and needing a comprehensive rewrite.
• The lead has not been kept in sync with the body of the article-- there is information in the lead which is nowhere to be found in the article.
• This statement in the lead doesn't even belong in this article ... it is not about AZ, rather all dementia. In 2015, dementia resulted in about 1.9 million deaths.[9]
• Sourced to 1998 and 2005!! In developed countries, AD is one of the most financially costly diseases.[19][20]
• There are 2,000 reviews in the last year alone listed for Alzheimer's, yet the article stagnates.
• The spoken Wikipedia link is 12 years old ... should be removed from article and placed on talk.
  • Done (t · c) buidhe 21:27, 29 July 2020 (UTC)

I will put this forward to FAR in about a month unless someone is able to rewrite and update. The list above is samples only-- a top-to-bottom rewrite and update is needed, and SandyGeorgia (Talk) 19:30, 29 July 2020 (UTC)

May I also note inconsistent spellings: ageing and aging are both used. (t · c) buidhe 19:43, 29 July 2020 (UTC)

And page numbers or section names are needed on lengthy journal articles. SandyGeorgia (Talk) 19:55, 29 July 2020 (UTC)

This is going to take a ton of work to clean up. Alzheimer's disease hypotheses change almost weekly. I'm going to recruit a neurobiologist that I know to do some redlining offline (she has no interest in editing Wikipedia), and maybe I'll give it a stab. I often refer to this article as one of the best medical articles on Wikipedia, if not the best. It has become stale. I think the original authors went on to other things once this became an FA. :( SkepticalRaptor (talk) 21:04, 29 July 2020 (UTC)

Remind your off-Wikipedia friend that they need to find the latest and highest quality secondary reviews (not primary sources) and rewrite the article to them. SandyGeorgia (Talk) 21:06, 29 July 2020 (UTC)

Citation style

This is the version that passed FAC, using the long and well established Diberri format of vancouver style author names with more than six authors truncated to three et al, to avoid chunking up the text in edit mode with 6,500 bites of template parameters that one has to edit around. I have restored the original citation style, per WP:CITEVAR, which should never have been changed. SandyGeorgia (Talk) 06:10, 6 September 2020 (UTC)

Planned work underway

See note here, and welcome User:Celmck! SandyGeorgia (Talk) 18:05, 31 December 2020 (UTC)

@Ajpolino and Celmck:, no edits since January 8; shall we move forward with a Featured article review? This article is quite badly dated. SandyGeorgia (Talk) 17:34, 12 March 2021 (UTC)

Initial suggestions for FAR

Hello all! I have been invited to help with this article and am working with User:Ajpolino and User:SandyGeorgia to try to adhere to standards and rules. Here are my notes on how I would edit this article. I will preface this by saying that really every section needs updated references, so I'm not going to repeat that for all of my notes below. I am happy to help find updated references for any sections that others are interested in working on, but could use help formatting them and inserting them where needed. Here, I mostly tried to focus on what content stands out to me as outdated, questionable, or inappropriate, and noted that I can start on the Causes, Pathophysiology, and Research Directions.

• Signs and Symptoms: This section is probably written okay but needs to be looked over and given updated references.
• Causes: I can work on this section. I think it needs slight reorganization and some cutting down to the most relevant information. Also I would like to present only the most well-known and supported hypothesis since there are so many listed now that sound a little random.
• Pathophysiology: I can work on this section. I may reorganize some of this information with the Causes and Research Direction sections to provide better flow, as well as clarify and elaborate on some points of the disease mechanism which are unclear.
• Diagnosis: I'm less familiar with all of this but definitely needs to be fact checked to see if diagnosis criteria are up to date. For example the main criteria it says were designed in 1984 and updated in 2007, so it's possible a lot has changed about AD diagnosis since then.
• Prevention: I think the organization and sections for this are probably good, but needs heavy updating. For example, this section mentions a lot of "potential" preventative measures that have since probably either been debunked or much further elucidated. Personally I would also add a heavy dose of sleep literature in the lifestyle section here.
• Management: Similar to the diagnosis section I am unfamiliar with this but can help with getting it more up to date. Considering there are no cures for AD, I doubt much of this will have changed.
• Prognosis: This could use a little reorganizing, but also an update to the risk factors for poor prognosis. Is there new information on disease features or risk factors that correlate with faster disease progression after onset? Also, needs fact checking for existing claims and updated references.
• Epidemiology: I think this should just be rewritten as a much shorter version based on a few newer references. It just needs to get across "there is a lot of AD everywhere, depends on age, sex, and location."
• History: This only describes the definition of Alzheimer's and its discovery, which looks fine as is. I would add history of research and clinical trials since there has been so much work on the disease now. There have been some major clinical trial failings over decades that really explain why it is hard to understand and treat this disease as well. Some of these are in the research directions but are over a decade old now, so I think it would be better to introduce them as history which will give context to why current research directions and trials have shifted towards different ideas.
• Society and culture: Not sure I'll have time to work on this, so at the least references could be updated.
• Research Directions:  I can work on this section. I think the following subsections should exist but will organize after consulting some reviews.
  1. Models:
     • Rodents
     • Cell lines: neurons, glia, ipscs
     • Biochemistry of abeta and tau
  2. Drug discovery (or Medication)
  3. Diagnostics: imaging, biomarkers
  4. Clinical trials: ongoing or planned

Other sections that currently exist: behavioral prevention, possible transmission, and infections. If anything these could be deleted.

• Further reading/external links: If it were up to me, I would probably delete the further reading and just go with external links that haven't been cited in the article, perhaps such as these.
  • Alz.org
  • NIH Alz data sheet
  • Alzforum
  • Alzfdn.org
  • Jackson labs alzheimer's page
  • Some book chapters from pubmed

So for now I can start on the Causes, Pathophysiology, and Research Directions sections. I can easily work on External links and eventually on the History section as well, and provide some help with finding updated references. Celmck (talk) 17:58, 8 January 2021 (UTC)

Hi, Celmck and welcome again! This is on my list, and I will catch up as I am able. (For an explanation of my editing style and "issues", see this thread.) So happy to have you on board! SandyGeorgia (Talk) 18:46, 8 January 2021 (UTC)

Celmck, apologies for the delay (such is the world of Wikipedia, where it can be hard to stay abreast of all of one's projects). I think your list above is amazingly comprehensive and shows remarkably quick adaption to how Wikipedia works. I am always willing to do the citation cleanup, so don't let that part concern you. Put in what you have, add the page number as a Template:Rp where you have it, and I will adjust (and you will learn as you go as you review my changes). I can certainly do the Society and culture part, but that is last priority. Best regards, SandyGeorgia (Talk) 16:58, 13 January 2021 (UTC)

Live Changes Request

Hi all! I'm a student at the BHSc program at McMaster, and User:Bharatss-SB,User:Joyjxu1 and I are currently taking a course where we have to update an article for a class assignment. We would love to edit this article, however our professor has concerns that the need for group consensus would significantly impede our progress. We were wondering if we could be granted permission to make live edits? No worries at all if this is not possible! — Preceding unsigned comment added by Joan1087 (talk • contribs) 13:04, 3 October 2021 (UTC)

Polysorbate 80

Why is it that we know Polysorbate 80 is used to enable medications to pass through the blood brain barrier. To me this seems to indicate Polysorbate 80 is recognized as being detrimental to the health of the blood brain barrier. Therefore we should use it with caution.

The problem is Polysorbate 80 is a recognized food additive and used in salad dressings and cheap ice cream. How is this use justified? Arydberg (talk) 01:29, 31 October 2021 (UTC)

Wiki Education Foundation-supported course assignment

This article was the subject of a Wiki Education Foundation-supported course assignment, between 7 September 2021 and 8 December 2021. Further details are available on the course page. Student editor(s): Joan1087, Bharatss-SB, Joyjxu1.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 13:58, 16 January 2022 (UTC)

Semi-protected edit request on 28 January 2022

Shareena3078 (talk) 08:19, 28 January 2022 (UTC)

as for being an medical editor intern along with working on alzheimer's disease article, I would like to point out or edit a few mistakes that I have noticed in the above article

 Not done: this is not the right page to request additional user rights. You may reopen this request with the specific changes to be made and someone will add them for you, or if you have an account, you can wait until you are autoconfirmed and edit the page yourself. Cannolis (talk) 10:24, 28 January 2022 (UTC)