Talk:Alzheimer's disease/Archive 9

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Diagnosis

As the daughter and daughter-in-law of dementia patients, I believe it would be beneficial to include a list of conditions that are known to cause dementia and the screening process for these conditions. For instance, thyroid disease must be excluded, but often only a TSH test is used and often it is only given once. Despite the fact that many practitioners use this test exclusively, there are many reasons why it shouldn't be depended upon as sole reason to exclude thyroid disease, which is common in the elderly: 1.)It is an indication of what the pituitary is doing, it doesn't measure thyroid blood levels. There are several reasons why the pituitary may not be reflecting the need for my thyroid hormone. There aren't good studies to suggest that TSH is a reliable indicator of thyroid disease 2.)Patients report a very large lag between indicating positive for thyroid disease and the onset of symptoms. 3.)There are very good, inexpensive tests available (free T3, free T4, and antibody tests for Graves' and Hashimoto's disease) which, together, will give a more accurate picture of the process of the disease. These tests cost much less than ongoing treatment of the disease. Under current guidelines, B12 deficiency should be ruled out but it the B12 serum test, at it's most common lab ranges, has a very high false negative rate. It should be used with a methylmalonic acid MMA) and homocysteine test, the levels of both will be high if body levels of B12 are low. My father is institutionalized now, but has been found to have both thyroid disease and B12 deficiency. Too much damage has been done by now, he can't come back.Kitkellison (talk) 22:18, 22 June 2010 (UTC)

I am sorry for the history of your father. It is true that we do not have a section on differential diagnosis. Maybe you could bring some reliable sources (See WP:MEDRS) on the subject and create some lines on the subject. The number of editors working at improving wikipedia articles is very limited so it would be difficult that it is done in the short time without your help. Bests.--Garrondo (talk) 07:16, 23 June 2010 (UTC)

Electrophysiological tests

The article is not comprehensive as it doesn't dicuss the electrophysiological tests used in the diagnostics (EEG, visual and auditory evoked potential) despite their great value as described for example in the article Dementia in the light of cognitive neurophysiology (in Slovene, has an English abstract) by Zvezdan Pirtošek. I'd add the material myself if I had just a bit more time (exam frenzy!). --Eleassar ^{my talk} 13:02, 3 July 2010 (UTC)

That source is pretty dated, but PMID 19204149 or PMID 19729174 might be more useful. LeadSongDog come howl! 15:51, 3 July 2010 (UTC)

I do not think is a common diagnostic tool for alzheimers disease, although I might me wrong; while it is true that they are of great value in investigation. Reviews on the diagnosis of AD do not usually mention them and therefore per WP:Weight the main article is most probably not the place for this info... Of course I can be convinced of the opposite with good secondary sources on diagnosis of AD. Bests.--Garrondo (talk) 20:30, 3 July 2010 (UTC)

PET imaging agents

In this edit's summary by Sbharris, the idea is advanced that the recent PET agents Pittsburgh compound B and flobetapir (a.k.a. 18F-AV-45) are little better than the older fluorodeoxyglucose (a.k.a. FDG). Is there some ref to support such an assertion? It would seem to a layperson (or a reader of those other articles) that the 20 minute half-life of Carbon 11 would be a significant constraint, requiring the imaging centre to be very close to the producer of the isotope, whereas 110 minutes for Fluorine 18 allows for courier service across a city or even further. The argument for florbetapir over the off-license fluorodeoxyglucose seems (per PMID 20447562) to be that as the former preferentially binds to amyloid plaques whereas the latter is taken up by all glucose-using cells, an "exquisitely high specific binding" to AD-affected tissue is obtained. LeadSongDog come howl! 17:20, 13 July 2010 (UTC)

Well, exquisitely high binding to plaques is obtained. But is that what you want? In preface, I certainly I have no doubt that anything that uses F-18 PET will be an improvement over C-11 PET, which has such a short half life for the isotope and any radiopharmaceutical that uses it, that it will never be more than a research tool. So the question is not whether Florbetapir should be better than PiB to image plaques-- probably it will be. However, that may be the wrong question, and it certainly needs to be proven. The problems are these:

• The loss of neurons in AD doesn't correlate with with plaque-density. It would be nice if it did, but it doesn't. That alone suggests that what you want is something that tells you where neurons are being hurt (dead and dying), rather than where plaques are. The question of whether beta-amyloid causes AD is not the same as whether or not plaques cause AD. It may well be that some other APP related mechanism well "upstream" of plaques causes AD, and in that case plaques would be no better marker for where things are bad, than hypometabolic or dead neurons.

• We already know that HMPAO SPECT and FDG-PET are about 85% specific and sensitive for diagnosing early AD. Moreover, both of them are better than any other known test for differentiating AD from other kinds of dementia (most particularly MID) in clinically demented patients. So far, nobody has proven that PiB is better, mostly because nobody has bothered to compare them. Thus, we already have tests which do more or less what PiB does and what Florbetapir hopes to do, and that have been tested and validated on far larger sets of patients than either of the latter two agents. Yet still not comparison trials. It's up to Florbetapir, as a possibly clinically relevant radiopharmaceutical, to show that it's a better agent for looking a various sets of possibly or certainly demented patients in the real world, not in a theoretical world which relies on a model for the pathophyiology of the disease that (for all we know) still may be wrong.

• Right now, 18F-AV-45 (Florbetapir) redirects to Avid Radiopharmaceuticals, a Wiki which in turn is full of insider corporate info that doubtless came from corporate insiders. It's mostly an ad. These guys have tested their stuff in a relatively few number of patients have published a few abstracts. One of them shows that patients with more plaques on scan have more plaques on autopsy. Well, I should hope so, but so what? Another shows that patients with more plaques are more likely to progress to clinical AD and dementia. Okay, but where's the control group of people with a poor SPECT or PET scan, and who were in the same condition? How were these people chosen to begin with? The devil is in the details.

• I'm a little miffed inasmuch as there's a LOT of data on SPECT and FDG-PET scanning of demented patients over the last 25 years, and I had a very hard time getting it into this article (I've been fought by people saying that AD is an autopsy diagnosis, and before that, the gold standard is neuropsych tests). Yet, one day after release of some abstract in a conference in Hawaii (Aloha to you too, pharma reps) there's more stuff in this article on Florbetapir than the other two modalities combined. At the very best, it's an unproven technology. And at worst, somebody with a monster COI has been adding a lot of data on this stuff.

• All of this corresponds with a pet-peave (okay, PET-peave) of mine, which is that demented patients often get MRI after MRI, while often their insurance companies will not pay for SPECT (which is only a little more expensive) and even more often, not pay for FDG-PET. Basically, costwise two MRIs = one FDG-PET, and I've seen many a patient who has a history of half a dozen head scans of one sort or another, and has been denied PET every time by insurance. Medicare didn't cover FDG-PET for dementia until 5 years ago! In the decade before that, so much money was wasted on MRIs in dementia that I wondered if there were some kind of conspiracy. SPECT and FDG-PET are still underused in dementia, in one case due to the Tc-99m shortage, and in the other due to equipment shortages. In such an environment I find the pushing of Florbetapir on Avid's investment capital to be more than a little irksome. I'm pretty sure that Avid will never test Florbetapir in a randomized prospective trial against SPECT and FDG unless they're forced to, and they won't be. That's how our system works, and that's one reason why it's imploding financially. So I admit that have personal feelings about this, and yet it's clear to me the bias is there. I think that if a NPOV article were written about nuclear medicine in the work-up of dementia or possible dementia, covering the material in proportion to its existence in peer-reviewed literature, most of the article would be on SPECT and FDG-PET, perhaps one paragraph would be on PiB, and perhaps two lines would mention Florbetapir. The amount of Florbetapir material in THIS article is certainly inappropriate, considering what we presently know of nuclear medicine and dementia. SBHarris 02:24, 14 July 2010 (UTC)

The web is abuzz with a connection between mad cow and alzheimers lately. An old story/theory being reborn. I first heard it from Jim Hightower some years ago. Scientific studies suggested this some years ago - some researcher even got a big prize I have read. Hightower's idea - he was ag commiisioner in TX at one time - comes from modern technology. At one time each cow was butchered slowly and inefficiently - now your hamburger mixes with lots of other cow carcasses so one bad cow is in effect multiplied. I believe 1 cow in 6,000,000 gets mad cow natuarlly ( they suspect some genetic basis - of coarse it may come from feed(ground up dead cows are put back into the stream using cattle feed) or other cow to cow contact. About 200,000 downer cows per year, cattle feed, giant hamburger batches and voila a disease that wasn't even known ( except for people who ate sheeps' brains, etc as delicasies) becomes a problem. Ya gotta love efficiency. 159.105.80.122 (talk) 11:18, 10 August 2010 (UTC)

Date of Alzheimer's description

Two years ago an editor changed the date in the lead from 1901 to 1906, with no explanation. As 1901 is the only date I've ever read for this, I've restored it to 1901. --Anthony (talk) 16:37, 29 October 2010 (UTC)

Perhaps you are confusing the date of the case with the date of his publication. The source cited at the end of that sentence clearly says that he described it in 1906. While the publication date is independently verifiable, the date of the case is not. Restoring.LeadSongDog come howl! 18:39, 29 October 2010 (UTC)

You're right. Sorry about that. She became his patient in 1901. Anthony (talk) 19:30, 29 October 2010 (UTC)

Not to worry. Others have been tripped up by that before. ;-) LeadSongDog come howl! 20:07, 29 October 2010 (UTC)

What is the average age of onset of Alzheimer's disease?

What is the average age of onset of Alzheimer's disease? Abdbdba (talk) 21:20, 30 October 2010 (UTC)

There's no direct answer possible, but see the "Epidemiology" section of the article. Please note that per wp:TPG, article talkpages are for the discussion of improvements to the article, not discussion of the topic. LeadSongDog come howl! 03:40, 31 October 2010 (UTC)

I asked this question at the Reference desk and received an answer: "It seems to be around 75 for the general population,[1][2] 72.8 for the genetically predisposed.[3]" It might be interesting to add this information to the article. Abdbdba (talk) 15:11, 31 October 2010 (UTC)

I'm not sure that the term "average age of onset" means very much, given that the demographics are largely determined by how many people live long enough to get into the susceptible range. The Epidemiology section contains much more useful information, as far as I can see. Looie496 (talk) 17:20, 31 October 2010 (UTC)

Average age for the onset of symptoms. Abdbdba (talk) 00:59, 1 November 2010 (UTC)

As more people live into their 80s and 90s, the average onset age will also increase, is that what you are saying Looie? Abdbdba (talk) 01:20, 1 November 2010 (UTC)

Yes, that's exactly what I was trying to say. Looie496 (talk) 16:32, 1 November 2010 (UTC)

Correction needed to Management Pharmacutical section

The Statement: "Patients with Alzheimer’s disease who have taken Huperzine A have improved general cognitive function, global clinical status, functional performance and reduced behavioural disturbance compared to patients taking placebos, according to a Cochrane Review.[164]" is incorrect. The Cochrane Review states "There is currently insufficient evidence of the effects of Huperzine A for Alzheimer's disease (AD)." and "There is therefore inadequate evidence to make any recommendation about its use. Rigorous design, randomized, multi-centre, large-sample trials of Huperzine A for AD are needed to further assess the effects." How can this be corrected? — Preceding unsigned comment added by SpectacledSpider (talk • contribs) 00:01, 17 December 2010 (UTC)

Fresh reviews to chew on re assessment and re prevention trials

... at [4] and [5] (both free fulltext).LeadSongDog come howl! 21:22, 10 November 2010 (UTC)

Recent sources

• Vaishnavi SN, Vlassenko AG, Rundle MM, Snyder AZ, Mintun MA, Raichle ME (2010 Oct 12). "Regional aerobic glycolysis in the human brain". Proc Natl Acad Sci U S A. 107 (41): 17757–62. PMID 20837536. {{cite journal}}: Check date values in: |date= (help)CS1 maint: multiple names: authors list (link)
• Vlassenko AG, Vaishnavi SN, Couture L, Sacco D, Shannon BJ, Mach RH, Morris JC, Raichle ME, Mintun MA (2010 Oct 12). "Spatial correlation between brain aerobic glycolysis and amyloid-β (Aβ) deposition". Proc Natl Acad Sci U S A. 107 (41): 17763–7. PMID 20837517. {{cite journal}}: Check date values in: |date= (help)CS1 maint: multiple names: authors list (link)
• Magnoni S, Brody DL (2010 Sep). "New perspectives on amyloid-beta dynamics after acute brain injury: moving between experimental approaches and studies in the human brain". Arch Neurol. 67 (9): 1068–73. PMID 20837849. {{cite journal}}: Check date values in: |date= (help)
• Mawuenyega KG, Sigurdson W, Ovod V, Munsell L, Kasten T, Morris JC, Yarasheski KE, Bateman RJ (9 December 2010). "Decreased clearance of CNS β-amyloid in Alzheimer's disease". Science. doi:10.1126/science.1197623.{{cite journal}}: CS1 maint: multiple names: authors list (link)

The above are touched on in Gina Kolati's lay summary here in the NY Times. Of these four papers, only PMID 20837849 is a review, but they may be enough to establish if Kolati's summary got it accurately or not. LeadSongDog come howl! 16:55, 14 December 2010 (UTC)

Other authors mentioned are Mucke L and Selkoe DJ, both of whom have published recent reviews in major journals that should be considered. LeadSongDog come howl! 18:15, 14 December 2010 (UTC)

Edit request from 173.53.25.235, 24 January 2011

{{edit semi-protected}} The word recognized is spelled incorrectly as "recognised' in the second paragraph, third sentence.

173.53.25.235 (talk) 08:04, 24 January 2011 (UTC)

Not done: please establish a consensus for this alteration before using the {{edit semi-protected}} template. "Recognised" is correct spelling in Commonwealth English. Wikipedia accepts several different varieties of English spelling, and so long as spelling is consistent within an article does not attempt to change spelling from one variety to another. See WP:ENGVAR.-gadfium 08:13, 24 January 2011 (UTC)

Alzheimer's disease versus AD

I have noticed that the two are used interchangeably throughout the article. I do not understand the rational for this, especially since there are other names / abbreviations besides AD noted. Is this correct to use two different proper nounds in the same article? meshach (talk) 01:54, 26 January 2011 (UTC)

While there are other names Alzheimer's disease is the most common as is its abbreviation. I have eliminated the abbreviations for other names in the lead so as to not confuse readers.--Garrondo (talk) 07:29, 26 January 2011 (UTC)

Thanks! meshach (talk) 17:54, 26 January 2011 (UTC)

Large page - how to split

So large it is slow to format and display. Shouldn't we split out some of the larger sections - Maybe start with Diagnosis, and Prevention ? Rod57 (talk) 13:07, 25 February 2011 (UTC)

Other species

This article says nothing about non-human species that get AD. My parents' cat has just been diagnosed by a vet as having the disease. Do any other species contract the disease too? Mjroots (talk) 08:55, 2 March 2011 (UTC)

Researchers would be delighted if true, but as far as I know as of today no animal (with the exception of genetically modified rodents) are known to suffer AD. That is reason why they use similar but not equal animal models.--Garrondo (talk) 10:10, 2 March 2011 (UTC)

Just going by what dad said to mum, which was the cat had AD. Whether what was meant by that is that the symptoms in the cat were similar to AD in humans or that the cat has contracted AD I don't know, as I'm not a vet and this is possibly straying into OR territory. That said, the Discovery Channel is a RS, and has covered the issue, with material taken from the Journal of Small Animal Practice, which also is presumably a RS. Mjroots (talk) 11:30, 2 March 2011 (UTC)

AD produces a specific pattern of damage on the brain which secondarily produces dementia. However dementia can be due to many origins. If you read the discovery source closely at no point do they talk about the brain damage but only about behavior (dementia). Moreover a quick search in pubmed gives no relevant results on the issue.--Garrondo (talk) 12:00, 2 March 2011 (UTC)

Liver cause

A study this month indicates the liver not the brain is the source of “amyloid” brain plaques associated with Alzheimer's disease. (KurzweilAI) Posting here for inclusion in the article... unless anyone objects? - RoyBoy 20:37, 12 March 2011 (UTC)

I object, and presumibly I will not be the only one: source proposed is a primary source in a mouse model of Alzheimer disease... I feel it is way too premature to add anything about it in this article. Take a look at WP:MEDRS for further info. --Garrondo (talk) 21:31, 12 March 2011 (UTC)

I have reverted per above your addition to the article. To have it in the article is scientific recentism.--Garrondo (talk) 21:36, 12 March 2011 (UTC)

I used the word "indicates", but did fail to note these are preliminary findings based on mice. As such I will defer to others on inclusion context, but I consider it clearly important enough to mention in some way. Yes its not ideal, but being Bold rarely is. Regarding recentism, do you understand the policy? It is about tilting the article, particularly with more coverage than is warranted for recent events. One sentence doesn't tilt the article, granted my addition could be improved... but come'on now. - RoyBoy 21:52, 12 March 2011 (UTC)

Apply the ten year test, the liver meme would clearly pass. - RoyBoy 21:55, 12 March 2011 (UTC)

Or not: many times experiments cannot be repeated, or as is in mice it may not translate into humans disease, or there can be a covariant explaining results or a 1000 things that can make this article be forgotten by next year. That is why a secondary reliable source on the issue (normally a review in a peer-reviewed journal) is required as threshold for inclusion in medical articles on wikipedia, specially for a disease as researched as AD and an article that at the moment is FA. Do you know how much research is produced every year in the mice model of AD: unless there is some indication of the importance of this article (and no, news are not enought for that) it should not be included: that indication are reviews on the issue and not your opinion on its importance. --Garrondo (talk) 22:11, 12 March 2011 (UTC)

So recentism need not apply, good. If verification fails, remove mention or preferably add that result in sentence 2, BTW still passes 10-yr test. "required as threshold", doesn't exist at Wikipedia, what led you to believe it does? But, being conservative with FA's is fine with me. "as researched as AD" ... this research happens to be notable. Reviews are strongly preferred if available, preliminary studies can and are routinely included with their caveats.

My opinion of course has no weight, and the failure to include "mouse model" is mine. However, I was trying to carry forward the strong findings of the researchers, for example: "confirming brain Aβ's peripheral origin". This isn't the first study I've read, this is strong language, sure many things can happen; but it's plain this specific finding won't be reviewed into obscurity. We are quite capable of noting the can's as they occur... flash in a pan, it remains one/two sentences; confirmation comes in, it expands. Leveraging peer-review that is the scientific method is a great way to keep noise creep / pseudoscience from good articles, but it can be over-leveraged.

Though I'd like to conclude by saying, excellent work on this article. It's a great FA! Including a sentence with caveats I promise won't change that, we can be patient for a review... but I fail to see the need. Remember, recent findings can be encyclopedic too. Regards, RoyBoy 06:47, 13 March 2011 (UTC)

Garrondo is right. Wikipedia is a tertiary source, an encyclopaedia, not the news. As a result, it will generally report facts after primary and secondary sources have. The given source has two problems: it is a primary research paper and it is a study of mouse models of Alzheimer's disease. The former cannot establish its own WP:WEIGHT, no matter how prestigious the journal is or the authors are. Nor can WP editors, regardless of their backgrounds, no matter how well they argue the case or how strong those arguments appear. The latter suggests great caution should be applied since the natural next research step is to see whether this is even relevant to human disease (which is what this article is about). The opinion that this mouse research might be notable or relevant to humans requires a secondary source to give it WP:WEIGHT. The question is: when discussing the cause of Alzheimer's disease, do our best secondary sources mention this research, and if they do, what importance do they place on it? At this stage, it is probably too early for that to have occurred. For a disease like Alzheimer's, which is a huge area of research and has a vast literature at all levels, there is absolutely no reason for WP to rely on primary research papers. Colin°^Talk 08:55, 13 March 2011 (UTC)

Your "absolutely no reason for WP" reminds me of why I believe you are both fashionably wrong. Too early for secondary source does not automatically equate to no mention. Yes mice be different; but the origin of Aβ's is unknown, if it was overturning established human findings, then I'd be in complete agreement with y'all. As such, I maintain it should be in the article.

In the end I am deferring to Garrondo, but this was a good opportunity to clarify actual Wikipolicy. I'm out of practice at Wikipedia, my addition to the article verifies that, but this isn't my first medical subject. - RoyBoy 16:15, 13 March 2011 (UTC)

This is actually a very good example of why Wikipedia has the policies it does. The link you provided is to a press release (basically a form of advertising), and the place the research was published, the Journal of Neuroscience Research, is a minor outlet with a pretty low impact factor. If the findings were really of major significance and didn't have any serious problems, the paper would surely have been published in a higher-impact journal. Looie496 (talk) 17:29, 13 March 2011 (UTC)

I'm well aware of the former (I used the journal cite for the article addition), as to the latter "minor outlet" I cannot speak to that (if accurate may simply reflect its a mouse study), but I'm pretty sure Wikipolicy doesn't either. So not pertinent in the long run. - RoyBoy 03:49, 16 March 2011 (UTC)

Five new genes identified

Can someone check out Nature Genetics 3 April online issue? It looks here as if we are in for a rash of new information. LeadSongDog come howl! 21:28, 4 April 2011 (UTC)

Ok, they are

• "Common variants at ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP are associated with Alzheimer's disease". 03 April 2011. doi:10.1038/ng.803. {{cite journal}}: Check date values in: |date= (help); Cite journal requires |journal= (help); Unknown parameter |authors= ignored (help) and
• "Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's disease". 03 April 2011. doi:10.1038/ng.801. {{cite journal}}: Check date values in: |date= (help); Cite journal requires |journal= (help); Unknown parameter |authors= ignored (help)

These are both letters, but were received by Nature on 9 and 27 Sep 2010 respectively. I suppose the WebMD bit could be considered a secondary source, but there will certainly more to follow.LeadSongDog come howl! 21:51, 4 April 2011 (UTC)

I don't think WebMD should be treated as a secondary source. The findings are certainly interesting (especially the two immune-related genes that showed the strongest effects), but probably not of such immediately obvious importance that they need to go directly into the WP article. Looie496 (talk) 22:54, 4 April 2011 (UTC)

Work needed

Hello everyone! This article currently appears near the top of the cleanup listing for featured articles, with several cleanup tags. Cleanup work needs to be completed on this article, or a featured article review may be in order. Please contact me on my talk page if you have any questions. Thank you! Dana boomer (talk) 15:41, 6 April 2011 (UTC)

Here are the tags that caused this:

• Two {{as of}} tags, indicating statements whose validity may change as time passes. In my opinion these tags can simply be removed, as the two statements are really no more time-limited than any other statement.
• One doi_brokendate in a {{cite journal}}. The DOI in question is 10.3233/BEN-2009-0232, and I have verified that this is the DOI shown on the journal's web page, so I don't know what to do about it.
• One {{Verify source}} tag that can probably be handled straightforwardly.
• One {{Primary sources}} tag, added I think by SandyGeorgia, indicating that the article relies too heavily on primary sources. The complaint is legitimate in my opinion, but this would be a huge ordeal to fix fully, and I do not believe it is sufficient all by itself to justify demotion of the article.

That's it, I believe. Looie496 (talk) 17:29, 6 April 2011 (UTC)

Fixed the doibroken. It wasn't. Much of the older "Imaging" section could be updated from this review:

• Weiner MW, Aisen PS, Jack CR Jr, Jagust WJ, Trojanowski JQ, Shaw L, Saykin AJ, Morris JC, Cairns N, Beckett LA, Toga A, Green R, Walter S, Soares H, Snyder P, Siemers E, Potter W, Cole PE, Schmidt M; Alzheimer's Disease Neuroimaging Initiative (2010 May). "The Alzheimer's disease neuroimaging initiative: progress report and future plans". Alzheimers Dement. 6 (3): 202-11.e7. PMC 2927112. PMID 20451868. {{cite journal}}: Check date values in: |date= (help)CS1 maint: multiple names: authors list (link)

LeadSongDog come howl! 22:52, 6 April 2011 (UTC)

Lancet

doi:10.1016/S0140-6736(10)61349-9 is a recent review in the Lancet that could be used for further work in the future. JFW | T@lk 13:49, 8 April 2011 (UTC)

I can access these articles, but I wish someday would come that these journals start allowing open access. These days when rumors and fringe theories are so prevalent, access to real data and real science is critical for medical education. I know these guys have to make money, and they can't have advertising from Big Pharma, I wish there was a middle ground. Abstracts are good, but not great, for information. I've seen abstracts with the typical wishy-washy conclusions, but then I read the full article, and the information is presented somewhat differently. OrangeMarlin ^{Talk• Contributions} 01:15, 20 April 2011 (UTC)

I agree. It is very frustrating. The Lancet wants $19.95 (Science Direct would charge $31.50!) for 12 pages. Does anyone actually pay for individual articles? With online publication, the actual costs of delivery are negligable. The abstract/summary of a review article ususally says nothing much anyway. I think a lot more people would contribute good work to WP if access to the full text was easier or free. On the other hand, the sooner the Daily Mail goes behind a paywall, the better. Sadly, that seems unlikely to happen[6]. Colin°^Talk 07:45, 20 April 2011 (UTC)

NIH diagnostic guidelines updated

Let me note that NIH has just released a statement saying that it has updated its guidelines for the first time in 27 years. As outlined in this release, the guidelines now recognize three stages: (1) preclinical; (2) mild cognitive impairment; (3) Alzheimer's dementia. Looie496 (talk) 00:24, 20 April 2011 (UTC)

Rewrite time? Or should we get a little past WP:RECENT? OrangeMarlin ^{Talk• Contributions} 01:12, 20 April 2011 (UTC)

Coconut oil?

Two words: coconut oil. I was reading about Dr. Newport's experience and it seems plausible. Speculative but I'm surprised I haven't seen it mentioned in the article talk archives. The pieces of the puzzle fit. (1) Absent from the Western diet because of the scare campaign on saturated fats leading to deficiency. (2) MCTs in coconut oil are metabolized like carbohydrates through the liver. (3) Ketonic backup energy source when brain has trouble using glucose. (4) A study found that high HDL lessens Alzheimer's risk by 60% but commentators make dumb interpretation saying to exercise and use olive oil(???) even though lauric acid in coconut oil raises HDL the most of any saturated or unsaturated fat. (5) Correlates to diabetes as well because refined sugars have replaced saturated fats causing insulin resistance leading to obesity.

Wow I surprise myself with the brilliance of my unified dietary disease hypothesis. So with one stone we solve AD, other neurological diseases, diabetes, CVD, and obesity (who knows maybe autism as well). Tell me when I win my Nobel. Not usable in Wikipedia of course—WP:MEDRS and all that—but I hope someone can connect the dots and take advantage of this insight. Lambanog (talk) 19:17, 23 March 2011 (UTC)

I'd nominate you. However, you will have to share the prize with me. OrangeMarlin ^{Talk• Contributions} 19:18, 23 March 2011 (UTC)

I particularly liked Ashton's line "And eating a diet low in cash high carbohydrates also can raise that money." I wonder what it means? Memo to self: {{cite cochrane}} "C"ool, {{cite news}} "N"ot. LeadSongDog come howl! 19:48, 23 March 2011 (UTC)

Oddly, the study Ashton failed to cite doesn't mention cash, lauric acid, or coconuts. I'm shocked.

• Reitz C, Tang MX, Schupf N, Manly JJ, Mayeux R, Luchsinger JA (2010 Dec). "Association of higher levels of high-density lipoprotein cholesterol in elderly individuals and lower risk of late-onset Alzheimer disease". Arch Neurol. 67 (12): 1491–7. PMID 21149810. {{cite journal}}: Check date values in: |date= (help)CS1 maint: multiple names: authors list (link) (primary source)

LeadSongDog come howl! 20:00, 23 March 2011 (UTC)

I'm shocked. Just shocked. And I was going to pop some popcorn in coconut oil. LOL. OrangeMarlin ^{Talk• Contributions} 20:02, 23 March 2011 (UTC)

Ah, now it's clearer. Newport has a single case that she can't even publish a case study upon because she is too intimately related, so she resorts to the popular press to get the word out. I suppose that might be construed as evidence, but in no way could it be treated as reliable. Time to move on.LeadSongDog come howl! 17:45, 24 March 2011 (UTC)

I've only now read the article and notice that the glucose deficiency, insulin resistance, AD as diabetes type 3, ketone replacement theory is not mentioned in the article. The article does not mention the brain manufactures its own energy. I've seen reviews of MCTs being used to treat epilepsy which seems related showing some promise. Why is this article weighted towards theories that don't work?

• Henderson ST. Ketone bodies as a therapeutic for Alzheimer's disease. Neurotherapeutics. 2008 Jul;5(3):470-80.

• Seneff S, Wainwright G, Mascitelli L. (April 2011). Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet. European Journal of Internal Medicine 22 (2): 134-140. PMID 21402242.

Lambanog (talk) 06:22, 31 March 2011 (UTC)

Fulltext of the review, on Seneff's MIT page, is here. No mention of coconut, but she elsewhere cites Henderson et al, which does mention glycerine and coconut or palm oil as ingredients in AC-1202, as this primary paper discusses. Note too the section on conflicting interests. Not quite the kind of impartial evidence we'd prefer to use, though I do find it interesting. LeadSongDog come howl! 20:06, 26 April 2011 (UTC)

See ketogenic diet. The very last paragraph briefly mentions Caprylidene, a medical food for "dietary management of the metabolic processes and nutritional requirements associated with mild to moderate Alzheimer's disease", with ketone-bodies-as-fuel as the proposed mechanism of action. Coconut oil is a source of MCT's and Caprylidene is an MCT, but I don't know how that particular product is manufactured. The cited prescribing information sheet lists some relevant research in this area. It was over a year ago that I last looked into this and there wasn't much on this new product, perhaps a new scholarly search will find some reviews? If you guys can help find some good sources on this area, I'd be interested. I'll have another look myself later.

MCT oil for epilepsy doesn't just "show some promise". It has been used for nearly 40 years and its efficacy is well documented, including a fairly recent RCT published in the Lancet Neurology. Colin°^Talk 07:16, 31 March 2011 (UTC)

DR6

Unless someone can cite evidence otherwise, the DR6 hypothesis comes from a single unreplicated study and does not belong on the main page, especially since it is described as the new update of the amyloid hypothesis, but should be in the discussion with other early unsupported and highly speculative hypotheses. The theory that the N-terminus of APP has anything to do with AD is easily refuted as it does not account for gamma secretase mutations. It simply does not have the evidence to merit it being on the main page when dozens of other much better supported ideas aren't mentioned.

http://www.ncbi.nlm.nih.gov/pubmed/20205669 — Preceding unsigned comment added by Jimray50 (talk • contribs) 21:07, 25 April 2011 (UTC)

Recent edits to Causes section

Changes by User:Indeblues are citing a ref that is on the borderline between primary and secondary. PMID 19075578 is a review, but on the point discussed it appears the user is basing the asserion on:

Recently, we also showed that RNA-bound iron plays a pivotal role in RNA oxidation in vulnerable neurons in AD [38]. Specifically, we found that rRNA provides a binding site for redox-active iron and serves as a redox center within the cytoplasm of vulnerable neurons in AD in advance of the appearance of morphological changes indicating neurodegeneration [38].

wherein ref 38 is PMID 15767256. I've softened the "cause" assertion, but left it in place pending other editor's input. Comments?LeadSongDog come howl! 15:21, 27 April 2011 (UTC)

Yo dog. I'm not an expert in these areas, so when I come to an article like this, let's say as a educated amateur, I look at the references, then who refers to the references. The problem with your two citations is that they're kind of recent, and there hasn't been enough back and forth in peer-reviewed articles to say whether this is, in fact, a viable mechanism. There hasn't been articles that make an obvious conclusion that this could be a definitive cause. In fact, I pulled up this one, PMID 20421693, I get a strong impression (even conclusion) that it's still very controversial. So, given undue weight and WP:RECENT issues, does even rate a mention? Maybe it should be pushed to a future research directions. Anyways, that's how this amateur views it.OrangeMarlin ^{Talk• Contributions} 15:55, 27 April 2011 (UTC)

New findings published in AARP newsletter

Could someone update this topic with the latest news? The plaque is to protect the brain from harm caused by increased proteins on the brain. The drugs previously used were to fight the plague, but the plaque was what protects the brain from the Darry give nature of the proteins. It is said that it will be at least 15 years until new drugs are ready for testing. I read this in AARP in this past year. —Preceding unsigned comment added by Slowpathtowisdom (talk • contribs) 14:09, 1 May 2011 (UTC)

Not really new, the hypothesis that the plaque buildup is a result of a protective mechanism is at least 5 years old but because of the editorial restrictions in place here you're not going to read about it in this article until it is old hat. More acceptable are theories that have been proven not to work. Lambanog (talk) 12:51, 6 May 2011 (UTC)

Got a wp:MEDRS to work from? LeadSongDog come howl! 14:12, 6 May 2011 (UTC)

Perhaps this and this recent review will make it clear that there is still no tested hypothesis which upon which a scientific consensus has formed, though some older ones have been ruled out or modified. LeadSongDog come howl! 14:58, 6 May 2011 (UTC)

"Editorial restrictions." You mean following verification through reliable sources? OrangeMarlin ^{Talk• Contributions} 01:44, 25 May 2011 (UTC)

May 24, 2011 I would like to update you about the hypothesis of alzheimer's disease as described by Dr. Herrup as being Age related. This article is found in Alzheimer's Research Forum. His hypothesis is based to the fact that there should be an initial injury, followed by an immune response then followed cellular death of specific neurons.My own Hypothesis explains about the dying of specific cells,then the immune response,finally death of specific cells and by amyloid deposits. These explains the Aging Process.Reference. U.S. Patent 7858602VRodrig110 (talk) 01:35, 25 May 2011 (UTC)

And once again, you're providing us with an unreliable citation, original research, and personal synthesis of other research. And please quit advertising your patent.OrangeMarlin ^{Talk• Contributions} 01:43, 25 May 2011 (UTC)

The look of it you have not even visited the website of Alzheimer's Research Forum, and you are already concluding that they are unreliable citations. Their website-- http://www.alzforum.org Re-Imagining Alzheimer's Disease by Dr. Karl Herrup et al from the University of Rutger's. Before giving any comment, kindly research first. You erased my Pathophysiology of Alzheimer's Disease even before you have researched on it.VRodrig110 (talk) 09:16, 25 May 2011 (UTC)VRodrig110 (talk) 09:20, 25 May 2011 (UTC)VRodrig110 (talk) 09:22, 25 May 2011 (UTC)

For your information this article is found in: http://www.jneurosci.org/content/30/50/16755.full Reimagining Alzheimer's Disease-- An Age Based HypothesisVRodrig110 (talk) 09:41, 25 May 2011 (UTC)

Since Journal of Neuroscience is publishing a description of the hypothesis you refer to, it certainly seems notable.

On this subject, for some articles where the cause of an illness is not fully understood, (Stuttering, Autism) there is a sub-article addressing etiology (Causes of stuttering, Causes of autism). Would it be appropriate for this topic to have such a sub-article where all the competing notable theories can be covered without concern about taking up undue space here? Biochemistry of Alzheimer's disease appears to be morphing into such a page; everything in the section Disease mechanism could be moved to Causes of Alzheimer's disease. --Anthonyhcole (talk) 11:16, 25 May 2011 (UTC)

Thank you for finally providing a wp:MEDRS that we can discuss rationally. More fully, it is

• Herrup K (2010 Dec 15). "Reimagining Alzheimer's disease--an age-based hypothesis". J Neurosci. 30 (50): 16755–62. doi:10.1523/​JNEUROSCI.4521-10.2010. PMC 3004746. PMID 21159946. {{cite journal}}: Check date values in: |date= (help); zero width space character in |doi= at position 9 (help) (PMC is embargoed until 15 June 2011)

This is a review covering a recent, plausible hypothesis that, as yet, has not been empirically tested. It could be useful as a reference for a statement in an etiology section or sub-article discussing current etiology theories, but it certainly is not going to support a statement that "AD is caused by xyz". Herrup's review has drawn two responses to date, one of which PMID 21167244 is available here in more detail (but not as a wp:MEDRS). I would suggest editors here take the time to read this review, but I think Anthony is right, it belongs in a sub-article that can discuss each of the current theories. I'm not certain that his proposed article title is correct, but it's reasonable as a starting point. One may observe that our articles on ALS and Parkinson's disease do not have subarticles for theories of causation, but those too might benefit from forking out that content. A general discussion of whether or not to fork content in such cases might be better held at Wikipedia talk:WikiProject Medicine. In any case, we would be left with a residual summary "Causes" section in this article. LeadSongDog come howl! 16:28, 25 May 2011 (UTC)

May 26, 2011 Thanks Anthony for your suggestions. The look of it if you place your competeting suggestions about the causes, biochemeistry and etc of Alzheimer's Disease, some wise guy will just erase it without even researching on the subject matter. The problem, if you are not qualified to do so, let administration decide before the subject matter is erased.We contributors spend lots of time preparing them, so whoever erases them should also do their part in researching on the subject matter.VRodrig110 (talk) 12:33, 26 May 2011 (UTC)VRodrig110 (talk) 12:34, 26 May 2011 (UTC)VRodrig110 (talk) 12:42, 26 May 2011 (UTC)

Huzerpine A

Under 'Management' the following is said about Huzerpine A, based on a Cochrane systematic review: Patients with Alzheimer’s disease who have taken Huperzine A have improved general cognitive function, global clinical status, functional performance and reduced behavioural disturbance compared to patients taking placebos, according to a Cochrane Review.[166]

I think this is overstating the conclusions of the review: perhaps change to: ... Huzerpine A may have improved..... and perhaps add: ... though the review highlighted the poor methodological quality of the small trials of huzerpine A, including problems with randomisation and blinding. Dhj davis (talk) 07:14, 23 June 2011 (UTC)

Following on from above: Hi Orangemarlin, I'm new, so am cautiously making new edits. I'd be grateful for the clarification. W.r.t. the edit on Huzerpine A, I didn't change the reference citation to the Cochrane -- I just edited the comment so that it reflected the concerns highlighted by the review (methodological biases etc). I felt that the article (as things stand) overstated the findings of the review. I see now that my edit might have appeared to be unsupported, but of course I'm referring to the review cited in the previous sentence. Perhaps I should cite the review again (at the end of both sentences)? — Preceding unsigned comment added by Dhj davis (talk • contribs) 11:59, 28 June 2011 (UTC)

I tidied it up. Normally where an entire para uses one ref we simply put the ref tag at the end of the para. I added a one-line quote from the plain-language summary in the Cochrane review. Cheers,LeadSongDog come howl! 12:28, 28 June 2011 (UTC)

Prevalence of familial forms? Contradiction with other article

The article claims "around 0.1% of the cases are familial forms of autosomal-dominant inheritance" yet the article early-onset Alzheimer's disease says "[early-onset AD] is an uncommon form of Alzheimer's, accounting for only 5-10% of all Alzheimer's sufferers. Approximately half the cases of early-onset Alzheimer's are Familial Alzheimer's disease" and later "[early-onset familial AD] is inherited in an autosomal dominant fashion". I don't see a way to reconcile the numbers; they appear to differ by a factor of at least 25. AxelBoldt (talk) 12:58, 13 July 2011 (UTC)

Senile Dementia

Hello. I am new to wikipedia but as a dementia historian feel as though I am capable of editing the history section of this page. Please could someone unlock it for me. Also I think there should be a page for 'senile dementia' and 'senility' and was wondering if somoeone could set these up, then I can edit the history sectionAnnatatton (talk) 12:18, 26 July 2011 (UTC).

I really think this needs its own page. For almost two centuries this was what dementia among older people was known as, to not acknowledge this and to mistakenly assume that just because Alzheimer's Disease was named in 1907 meant that that's what the disease was called then is an error. Please Wikipedia put senile dementia in your encyclopaedia, and while you're at it, please put senility in too. 78.105.115.109 (talk) 15:47, 26 July 2011 (UTC)

We have an article on senile dementia (which is a state caused by many different diseases). Could you maybe try searching the encyclopedia before complaining? SBHarris 16:07, 26 July 2011 (UTC)

Hmm, a bit bitey? Anyhow, senile dementia is a redirect to dementia, as is Senile Dementia. Shouldn't we have a non-senile dementia article (and/or section) addressing causes unrelated to age? LeadSongDog come howl! 17:23, 26 July 2011 (UTC)

Sigh. Yes, it's a redirect. So? The article dementia IS the article on senile dementia as well. It's a general article on dementia, both on those types where age is a risk factor and those where it isn't. But since the two are so difficult to separate, if we have two articles on the many causes of dementia, one for those where age plays a role and one where it doesn't not, somebody would be suggesting that they be merged. Dementia is a syndrome, after all, not a disease. Would we have two articles on senile and non-senile arthritis? No, it's too general a topic to break down like that. SBHarris 19:18, 26 July 2011 (UTC)

Fine, a section within dementia, then, to address CTE, rabies, and other collected causes, distinct from Alzheimer's, Lewy body, vascular etc? I'm thinking we should essentially reflect the ICD-10 breakdown (not that I've yet checked it). LeadSongDog come howl! 20:54, 26 July 2011 (UTC)

Well, F00-F03 would apply, though ICD-10 doesn't use the adjective "senile". We're essentially talking about the F02 and to a lesser extent the F03 sections. LeadSongDog come howl! 21:10, 26 July 2011 (UTC)

Regarding editing the article, you will be able to do so without any special help as soon as you have made a total of 10 edits of any sort -- currently you have only made two. Perhaps you could use those edits to discuss here the sorts of changes you would like to make. Looie496 (talk) 17:40, 26 July 2011 (UTC)

To all responses: Yes I definitely think SBHarris has been 'bitey' towards me and it's not something I take kindly to and makes me more determined to contribute and alter your frankly dogmatic views SBHarris. Because I am a dementia historian, specifically dementia among older people this is a major issue for me. Alzheimer and Krapelin made a fundamental, major error in naming Alzheimer's disease in 1907 as a presenile dementia when it wasn't and this took back geriatric and psychiatry medicine about seventy years. — Preceding unsigned comment added by Annatatton (talk • contribs) 08:29, 27 July 2011 (UTC)

I'm not aware of having any "dogmatic views" in this area. It's extremely common in science that common things pass unnoticed until some scientist first notices an extreme example (which is thought rare) and as people look they gradually realize that what was thought rare is more the rule than the exception. Imagine the first people who noticed that heavy friction slows some kinds of motion-- they didn't set the whole field of kinetics back thousands of years by immediately failing to generalize. That's what a Newton is for, and Newtons are rare.

Alzheimer did nothing but a service to the field by adding a little stone of knowledge. Indeed, since plaques and tangles are found in the brains of elderly people with no clinical dementia at all, it's a matter of amounts for the tangles, and it's not even that for the plaques (since their concentration does not correlate in brains areas with amount of damage and neuron loss). So it's amazing that Alzheimer et al. managed to do as well as they did. Science stumbles toward the light. In Alzheimer's time, dementia was thought to be a consequence of aging like loss of elastic tissue and arthritis. The fact that not every last person got it, was taken only as evidence that were lucky enough to die before they inevitably did. And the cause was thought vascular since Virchow (who was not so dumb, since vascular causes and cholesterol metabolism do clearly play a major role for many people).

Nobody could have been expected to throw out this paradigm and set it all right in 1907. That's expecting far, far too much of the way science works. It is also retrospectocope thinking. Okay, critic, you tell ME why plaques don't correlate with neuron loss in brain areas. Not so easy when you don't have the answer in front of you, is it? Nobody knows, right now. So be humble and don't judge scientists. If you work in science, you know how it goes. If you don't, you should take my word for it. SBHarris 07:36, 10 August 2011 (UTC)

Sage Missing

There's no mention of Sage on this page. I believe it should be listed along with other cholinesterase inhibitors. Turmeric is listed along with other anti-inflammatory drugs. Currently it only lists FDA-approved drugs, but it probably should mention others that have been proven effective like Sage (or for example Cognex) but aren't approved (due to liver damage). Carl Kenner (talk) 05:21, 10 August 2011 (UTC)

Nutritional Support for Alzheimer’s Disease

Nutritional support for Alzheimer’s disease should be added as a subsection under Management (section 6) of this article and should encompass to categories, medical foods and feeding tubes. [1]

In the United States, a medical food is categorized and regulated as a food rather than a drug. A medical food is different from other foods, namely conventional foods and dietary supplements. The 1998 Orphan Drug Act [21 US Code 360ee (b) (3)] defines a medical food as a food “formulated to be consumed or administered enterally under the supervision of a physician and which is intended for the specific dietary management of a disease or condition for which distinctive nutritional requirement, based on recognized scientific principles, are established by medical evaluation.”[2]

Alzheimer’s disease seems to be a condition with “distinctive nutritional requirements.” In order to be amenable to a medical food intervention, Alzheimer’s disease must (1) result in an impaired capacity to ingest, digest, absorb or metabolize ordinary foodstuffs or certain nutrients OR (2) have unique, medically determined nutrient requirements AND (3) require dietary management not achievable by normal diet modification alone. [3] During the course of Alzheimer’s disease, persons lose the independent ability to obtain, prepare, and ingest food. An evolving body of scientific literature is pointing to Alzheimer’s disease being associated with chronic inflammatory processes, changes in energy metabolism, and alterations in food preferences that require unique nutrient needs that cannot be overcome by simple modification of the normal diet. [4, 5, 6]

A medical food for the nutritional needs of mild-to-moderate Alzheimer’s disease patients (AC-1202, Axona®; Accera, Inc., Bloomfield, CO, USA) became commercially available in the United States in 2009. [1] AC-1202 is a medium chain triglyceride product composed of caprylic acid (C8:0) and glycerin. The rationale for AC-1202 is that glucose hypometabolism by brain neurons occurs in Alzheimer’s disease. Neurons with difficulty processing glucose may be able to use ketone bodies as an alternate fuel sources. Medium chain triglycerides such as caprylic acid, which are metabolized into ketone bodies, are not present in sufficient quantities in the regular dietary intake of coconut oil or palm kernel oil to meet the needs of persons with Alzheimer’s disease. In a 3-month, multicenter, randomized, double-blind, placebo-controlled, clinical trial of the safety and efficacy of AC-1202 in 152 participants with mild-to-moderate Alzheimer’s disease already taking currently available United States Food and Drug Administration treatments were randomized to daily intake of 20 grams of AC-1202 powder shaken and blended in 4-8 ounces of water or a matching placebo. [7] Compared to placebo, 90-day treatment with AC-1202 was associated with improvement on the Alzheimer’s Disease Assessment Scale Cognitive subscale (ADAS-Cog), a commonly used research measure of cognitive function but not the second primary endpoint of the Alzheimer’s Disease Cooperative Study Clinical Global Impression of Change scale, a commonly used measure of clinically detected global change in performance. [7] In a pre-specified analysis, the AC-1202 seemed to be beneficial in the group of Alzheimer’s disease participants without an apolipoprotein E ε4 allele, a genetic risk factor for Alzheimer’s disease.[7] The most common adverse events were gastrointestinal upset (49% in the treatment group versus 27.3% in the placebo group). [7] Further studies of AC-1202 are needed to replicate and validate these findings.

Other medical foods for Alzheimer’s disease are currently under various stages of development. [8, 9, 10]

Medical foods may be a novel pathway to complement other management interventions for Alzheimer’s disease. Issues still need to be resolved before medical foods become widely accepted as a management modality for Alzheimer’s disease. Researchers must continue to explore and define the unique nutritional needs associated with all stages of Alzheimer’s disease from the asymptomatic phase to the advanced phase. Medical food developers need to provide the best scientific justification for bringing their product to the market as a medical food for Alzheimer’s disease. Government regulators and policy makers need to consider requiring confirmatory research before or after a medical food for Alzheimer’s disease is brought to market. Public and private healthcare payers need to encourage the conduct of comparative effectiveness research. Clinicians, advocacy groups, and patients need to provide feedback on the safety, efficacy, and tolerability of medical food interventions in the post-marketing period.

1. Shah RC. Medical foods for Alzheimer’s disease. Drugs Aging 2011;28(6): 421-428. PMID 21534638
2. US Food and Drug Administration. Medical foods: overview [online]. Available from URL: https://www.fda.gov/Food/FoodSafety/Product-SpecificInformation/MedicalFoods/default.htm [Accessed 2011Aug11]
3. US Food and Drug Administration. Guidance for industry: frequently asked questions about medical foods May 1997-revised May 2007[online]. Available from URL: http://www.fda.gov/Food/GuidanceComplianceRegulatoryInformation/GuidanceDocuments/Medical Foods/UCM054048 [Accessed 2011Aug11]
4. Wang PN, Yang CL, Lin KN, et al. Weight loss, nutritional status and physical activity in patients with Alzheimer’s disease: a controlled study. J Neurol 2004; 251:314-320. PMID 15015012
5. Tamura BK, Masaki KH, Blanchette P. Weight loss in patients with Alzheimer’s disease. J Nutr Elder 2007;26:21-38. PMID 18285291
6. Ferreira IL, Resende R, Ferreiro E, et al. Multiple defects in energy metabolism in Alzheimer’s disease. Curr Drug Targets 2010;20:1193-1206. PMID 20594180
7. Henderson ST, Vogel JL, BarrLJ, et al. Study of the ketogenic agent AC-1202 in mild to moderate Alzheimer’s disease: a randomized, double-blind, placebo-controlled, multicenter trial. Nutr Metabl (Lond) 2009;6:31. PMID 19664276
8. Scheltens P, Kamphuis PJ, Verhey FR, et al. Efficacy of a medical food in mild Alzheimer’s disease: a randomized, controlled trial. Alzheimers Dement 2010;6:1-10.e1. PMID 20129316
9. Newsome D. Copperproof-2: prospective, randomized, double-blind, placebo-controlled clinical trial compairing the effects of a novel once-daily oral zinc cysteine preparation on zinc and copper parameters in mild cognitive impairment and Alzheimer’s disease [ClinicalTrials.gov identifier NCT01099332]. US National Institutes of Health, ClinicalTrials.gov [online]. Available from URL: http://www.clinicaltrials.gov [Accessed 2011Aug11].
10. Parachikova A, Green KN, Hendrix C, et al. Formulation of a medical food cocktail for Alzheimer’s disease: beneficial effects on cognition and neuropathology in a mouse model of the disease. PLoS ONE 2010; 5(11):e14015. PMID 21103342

Rajcshah (talk) 14:07, 14 August 2011 (UTC)

I think that is far too much detail for this article, although it would make a good starting point for a subarticle on Nutritional support for Alzheimer's disease. For this article, I think it would be reasonable to add one not-too-long paragraph to the Management section, referenced to your review paper. Note that Wikipedia differs from the academic literature in that we prefer to use secondary sources (such as review papers) for references, rather than referencing primary sources such as clinical study papers; see WP:MEDRS for more information. This is because large numbers of references make an article difficult to maintain, and because when primary studies draw conflicting conclusions only an expert is capable of weighting them appropriately. Looie496 (talk) 17:21, 14 August 2011 (UTC)

I appreciate the comments and suggestions as I am new to using Wikipedia. As requested by the editor, I have adjusted the article to include PMIDs and to change a reference regarding the commercialization of the product. As far as a shortened version, I would suggest the following:

Medical foods, which are regulated as foods rather than as drugs, may be a novel pathway to complement other management interventions for Alzheimer’s disease (AD). AD may be viewed a condition with distinct nutritional requirements. AD seems to (1) result in an impaired capacity to ingest, digest, absorb or metabolize ordinary foodstuffs or certain nutrients OR (2) have unique, medically determined nutrient requirements AND (3) require dietary management not achievable by normal diet modification alone. A medical food for the nutritional needs of mild-to-moderate AD patients (AC-1202, Axona®; Accera, Inc., Bloomfield, CO, USA) became commercially available in the United States in 2009. Other medical foods for AD currently are under various stages of development. Issues still need to be resolved before medical foods become widely accepted as a management modality for AD. Researchers must continue to explore and define the unique nutritional needs associated with all stages of AD from the asymptomatic phase to the advanced phase. Medical food developers need to provide the best scientific justification for bringing their product to the market as a medical food for AD. Government regulators and policy makers need to consider requiring confirmatory research before or after a medical food for AD is brought to market. Public and private healthcare payers need to encourage the conduct of comparative effectiveness research. Clinicians, advocacy groups, and patients need to provide feedback on the safety, efficacy, and tolerability of medical food interventions in the post-marketing period. [1]

1. Shah RC. Medical foods for Alzheimer’s disease. Drugs Aging 2011;28(6): 421-428. PMID 21534638

Rajcshah (talk) 23:04, 23 August 2011 (UTC)

resource

Chimp brains don’t shrink; Study indicates brain withering may be uniquely human by Laura Sanders August 27th, 2011; Vol.180 #5 (p. 8) Science News. 99.181.138.215 (talk) 02:27, 18 August 2011 (UTC)

Causation (answered)

Currently, under "Causes" the article has "Several competing hypotheses exist trying to explain the cause of the disease. The oldest, on which most currently available drug therapies are based, is the cholinergic hypothesis, which proposes . . ."

Under "Genetics", we find "The vast majority of cases of Alzheimer's disease are sporadic, meaning that they are not genetically inherited although some genes may act as risk factors . . .".

I plan to add a sentence to the "Causes" section as follows: "The cause for most Alzheimer's cases is still essentially unknown. Several competing hypotheses exist trying to explain the cause of the disease. The oldest . . ."

Comments? Objections? -- Jo3sampl (talk) 13:47, 29 September 2011 (UTC)

I think that first sentence is somewhat misleading. Many people feel that we do know the cause of AD: the accumulation of plaques and tangles. What is not known is what causes plaques and tangles to accumulate in some people but not others. Also let me note that the science on Alzheimers has been advancing quite rapidly, and it is possible that some statements in the article are out of date. Looie496 (talk) 14:18, 29 September 2011 (UTC)

Thanks for the response! At http://www.ncbi.nlm.nih.gov/m/pubmed/11065271/ we see "Contrary to common concepts, the brain in Alzheimer's disease (AD) does not follow a suicide but a rescue program. Widely shared features of metabolism in starvation, hibernation and various conditions of energy deprivation, e.g. ischemia, allow the definition of a deprivation syndrome which is a phylogenetically conserved adaptive response to energetic stress. . . . [C]umulative evidence, taken together compelling[ly] suggests that senile plaques are the dump rather than the driving force of AD. . . .". At http://www.mayoclinic.com/health/alzheimers-disease/DS00161/DSECTION=causes, there's "Scientists believe that for most people, Alzheimer's disease results from a combination of genetic, lifestyle and environmental factors that affect the brain over time. Less than 5 percent of the time, Alzheimer's is caused by specific genetic changes that guarantee a person will develop the disease. . . . While the causes of Alzheimer's are not yet fully understood, its effect on the brain is clear."

I'll post a request for advice at Wikiproject Neurology, too. Thanks again. -- Jo3sampl (talk) 17:53, 29 September 2011 (UTC)

Well, a decade is a long time in this field, I wouldn't give too much weight to a 2000 paper. Have a look at PMID 21871538 and PMID 20420489. Though it may take a while to solidify, a consensus seems to be emerging lately that various insults and/or genetic factors can cause oxidative stress to the mitochondria that power nerve cells, causing disfunction of these mitochondria that in turn triggers a viscious cycle that leads to further reactive oxygen stress, AB accumulation, and so on.

Wandering deep into wp:SYNTH territory, newer studies into interventions in the early development of the disease are looking at protecting the mitochondria from oxidative stress before the cycle is established. With improvements in imaging (PMID 21471273 refers) it is now possible to assess candidate interventions in high risk groups in advance of symptoms, which implies much quicker feedback in the development of drug candidates than was previously possible. LeadSongDog come howl! 21:10, 29 September 2011 (UTC)

Thank you! I read those summaries, and did a little more looking for reliable sources. I have now convinced myself that the causes of non-familial Alzheimer's are still unknown, although ideas and studies abound. I'm not sure the causation summary is truly current, but there's a 2011 date on the page http://www.med.nyu.edu/adc/forpatients/ad.html#causes and I'm sure NYU Medicine is a reliable source. The page has this:

The cause of Alzheimer's disease is not yet known, but scientists are hoping to find the answers by studying the characteristic brain changes that occur in a patient with Alzheimer's disease. In rare cases when the disease emerges before the age of sixty-five, these brain changes are caused by a genetic abnormality. Scientists are also looking to genetics as well as environmental factors for possible clues to the cause and cure of Alzheimer's disease.

I'll try for a response at the Neurology and Medicine projects, then plan to modify the aricle as above unless I hear otherwise from the Neurology or Medicine wikiprojects. -- Jo3sampl (talk) 19:00, 30 September 2011 (UTC)

Posting from WikiProject Medicine:

Yes I think it is fair to say the cause is unknown except for a few cases. The pathophysiology is fairly well understood though but not the cause. — Preceding unsigned comment added by Jo3sampl (talk • contribs) 22:07, 30 September 2011 (UTC)

The source you cited is at least seven years old. We shouldn't take it as authoritative in representing today's understanding. LeadSongDog come howl! 05:45, 1 October 2011 (UTC)

Alzheimer's Association ref. added. -- Jo3sampl (talk) 16:17, 1 October 2011 (UTC)

I agree that the source is out of date. It's wrong on the prevalence of AD too. The statements are not verifiable. Although NYU is a fine institution, the source page is not a valid source. Although the cause of AD has not been pinned down in sporadic cases, there is mounting evidence that amyloid plaques are key (certainly not irrelevant). You need to find a very recent review, preferable from the primary medical literature--published this year. Presto54 (talk) 07:39, 13 October 2011 (UTC)

Edit request from Feelsky, 2 October 2011

Uh, no. I'm hiding this because it is pure spam. Looie496 (talk) 15:15, 2 October 2011 (UTC)
The following discussion has been closed. Please do not modify it.
I would like to add section about Alzheimer's Enbrel Treatment and Training in Nicaragua "Alzheimer's Enbrel Treatment and Training Alzheimer’s Enbrel perispinal injection treatment and training is now available in Nicaragua. Perispinal injection technique for administering the drug Enbrel (Etanercept) is taught at our center. This procedure reverses Alzheimer’s dementia, resulting in an immediate and dramatic restoration of memory, mood, and cognitive function. Our Alzheimer’s Enbrel perispinal injection treatment not only restores short term memory, but our clients also experience improved posture and balance, and are more likely to initiate conversation and respond to questions with multi-sentence answers. One only needs to look into their eyes to notice a striking change. Caregivers report “she is back,” and “her behavior and personality resemble the way she was three years ago.” Neurological Wellness Center http://reversealzheimersnow.com/ provides Enbrel perispinal injection training, enabling caregivers to become proficient in the administration of this life-changing Alzheimer’s dementia therapy. Our Alzheimer's Enbrel treatment improves and restores memory, and reduces dementia, reversing the effects of Alzheimer's disease. We enable our clients to experience for themselves dramatic improvements in memory, mood and cognitive function. During 4 hour caregiver is allowed to practice on our model (a living adult) until they become proficient in all aspects of the perispinal injection procedure. Each caregiver is taught to administer the following cognitive function and mood assessment tools: TYM: Test Your Memory, MMSE; Mini Mental Status Exam, NIS Neuropsychological Impairment Scale and the Mini Oxford Happiness Questionnaire. They are given master copies of these assessment tools for baseline scoring and effective measurement of the improvement in memory, mood and cognitive function. " And add external link: http://reversealzheimersnow.com/ Neurological Wellness Center site Feelsky (talk) 14:33, 2 October 2011 (UTC)

Edit request from , 12 October 2011

{{edit semi-protected}} I would like to add the following paragraph in the section Disease mechanism: Lately, scientists published another new hypothesis concerning the mitochondrial dysfunction due to problematic inner mitochondrial membrane [1]. Their hypothesis is based on the fact that the inner mitochondrial membrane is a natural superconductor. Subsequently, any case of inappropriate intra-structure is followed by high level transmembrane proton concentration, blocking actually the natural pathway of producing ATP. Due to the action of complexes during the flow of electrons, protons are unequally distributed on both sides of the inner mitochondrial membrane. Therefore, the mitochondrial matrix becomes poorer in protons. Due to the action of the respiratory chain complexes, the energy of electrons is temporarily stored in the form of electrochemical energy potential. This form of energy will be restored via the returning of protons through particular channels of the internal membrane in the matrix and will be used to cover energy needs. In other words, the electrochemical potential, or proton-stimulatory power, corresponds to the tendency of the protons to be restored to their initial locations, in order to achieve equilibrium and reset the imbalance of the protons. The size of this energy is proportional to the size of the difference between the concentrations of protons on both sides of the membrane. While the final reaction in the respiratory chain is taken place, when ‘electric thromboses’ occurs, the superconductivity of electrons is destroyed and no pair of electrons are transferred. It is obvious that the existence of electric complexes can be either temporary or permanent, with adverse impacts on nerve cells.

[1] Alexiou A, Rekkas J, Vlamos P. Modeling the mitochondrial dysfunction in neurogenerative diseases due to high H+ concentration, Bioinformation 6(5)173-175, 2011

Bioinfo12 (talk) 20:38, 12 October 2011 (UTC)

That's PMC 3124800. It appears to be a primary source, but will no doubt stimulate a response before long, at which time there will be a secondary source to work with. There is wp:NODEADLINE, so hang on.LeadSongDog come howl! 21:27, 12 October 2011 (UTC)

That's not written at a level that is appropriate for this article, regardless of whether better sources come along. This top-importance and very widely read article must try to stay accessible to a broad range of readers. Looie496 (talk) 15:13, 13 October 2011 (UTC)

Per the above comment, and WP:RECENT, and Wikipedia:Make technical articles understandable, this request is declined for now. If there is consensus here for the request, please use a further {{edit semi-protected}}.  Chzz  ►  00:04, 14 October 2011 (UTC)

Prion research on Alzheimer's

Prions may cause Alzheimer's. Could someone add something on this. http://www.nature.com/news/2009/090225/full/news.2009.121.html --Ericg33 (talk) 01:45, 2 November 2011 (UTC)

The paper in question only gives evidence that prion proteins play a role in Alzheimers, not that they cause it. In any case that's a primary research article and therefore not a good source for us to use. However it has been very widely cited, and is discussed in at least two reviews, including PMID 20698011 and this paper from PubMed Central. Looie496 (talk) 02:19, 2 November 2011 (UTC)

Prognosis

"Because AD cannot be cured and is degenerative, the sufferer relies on others for assistance."

This is no longer true cause Marijuana is linked to preventing and treating Alzheimer's disease: Americans for Safe Access also has links to research studies suggesting that cannabis may help in the treatment or prevention of Alzheimer's disease and cancer, while the International Association for Cannabis as Medicine highlights the following medical uses

Alzheimer's disease is the leading cause of dementia among the elderly, and with the ever-increasing size of this population, cases of Alzheimer's disease are expected to triple over the next 50 years.

Consequently, the development of treatments that slow or halt the disease progression have become imperative to both improve the quality of life for patients as well as reduce the health care costs attributable to Alzheimer's disease. Here, we demonstrate that the active component of marijuana, Δ9-tetrahydrocannabinol (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid β-peptide (Aβ) aggregation, the key pathological marker of Alzheimer's disease. Computational modeling of the THC-AChE interaction revealed that THC binds in the peripheral anionic site of AChE, the critical region involved in amyloidgenesis.

Compared to currently approved drugs prescribed for the treatment of Alzheimer's disease, THC is a considerably superior inhibitor of Aβ aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease. — Preceding unsigned comment added by 94.76.168.75 (talk) 16:05, 28 November 2011 (UTC)

Also known as

Alzheimer's disease (AD), also called Alzheimer disease, senile dementia of the Alzheimer type, primary degenerative dementia of the Alzheimer's type, simply Alzheimer's (as a stand-alone attributive adjective noun), and folk-etymological names such as "old-timers' disease", is the most common form of dementia is an awfully long sentence, especially considering there are only six words of fact in it! Do we really need all of those aka's, all but one of them with "Alzheimer" in them, in the first sentence? If it was also commonly known as "Joe Bloggs' disease" or "brain-rot" it would be worth including aka's so that readers would know they were on the page they were looking for, but as it is the reader is thoroughly befuddled before he or she gets to the all-important "...is the most common form of dementia." Why not a separate "Name" section if all of those variants are worth mentioning? 86.41.20.6 (talk) 11:17, 15 November 2011 (UTC)

I agree. Moved the names; separate section might be better. -- Jo3sampl (talk) 02:18, 17 November 2011 (UTC)

I have created a separate section for reasons apparent when you read it. The two modern terms, Alzheimer's disease and Alzheimer disease, are equivalent and almost equally common in the literature, like Parkinson's disease and Parkinson disease. Both should be left in the lede as it would be a big fight to figure out which to drop. The article could be renamed also, but the same applies. SBHarris 02:37, 17 November 2011 (UTC)

Edit request on 9 December 2011

11. Research directions One of the most recently published findings into the causes of Alzheimer's was completed by Geoff Faulkner and his team of scientists at the Roslin Institute. In an article published October 30, 2011, Faulkner presented evidence showing that retrotransposons are responsible for Alzheimer’s and other neurodegenerative diseases(1). Retrotransposons are active in many genetic mutations, and comprise a large portion of all nuclear DNA(2). Faulkner’s studies show that when retrotransposons insert themselves into the DNA of brain cells, they alter that DNA, thereby potentially coding for Alzheimer’s and other neurodegenerative diseases. If scientists were able to find a way to prevent this insertion of retrotransposons, the potential to cure almost any neurodegenerative disease may be on the horizon.

1. "Somatic retrotransposition alters the genetic landscape of the human brain," Nature: International Weekly Journal of Science, 30 Oct. 2011, Web. 1 Nov, 2011,www.nature.com/nature/journal/vaop/ncurrent/full/nature10531.html. 2. "Retrotransposons Research”, College of Biological Sciences, University of Minnesota, 8 May 2010, Web, 17 Nov. 2011, http://www.cbs.umn.edu/labs/voytas/retrotransposons/.

71.237.99.247 (talk) 23:22, 9 December 2011 (UTC)

This is interesting but I would not say that it is guiding current research directions in the AD field. The amyloid hypothesis and its more recent modifications have been the basis of drug development and much of the animal and cell work to date. SilverSteelWolf (talk) 16:10, 12 December 2011 (UTC)

Yes, interesting. But it would be WP:SYNTH to state that this research had anything to do with Alzheimer's disease at this time. And we neither predict the future, or reach non-published conclusions in this encyclopedia. But thanks for giving us a head's up. OrangeMarlin ^{Talk• Contributions} 17:32, 12 December 2011 (UTC)

Edit request on 27 December 2011

I am the webmaster for the National Institute on Aging, and we just redesigned our web site, so many of the citations are now broken. I don't currently have a need to make 8 additional edits to unprotected pages, which I would need to do in order to be able to update this semi-protected page. My apologies, I hope I will be able to contribute more eventually.

Please change this:

• Alzheimer's Disease Research Centers National Institute of Aging

to this:

• Alzheimer's Disease Research Centers National Institute of Aging

this referenced URL: Gradually, bodily functions are lost, ultimately leading to death. "Understanding stages and symptoms of Alzheimer's disease". National Institute on Aging. 2007-10-26. Retrieved 2008-02-21. to this: Gradually, bodily functions are lost, ultimately leading to death. "About Alzheimer's Disease: Symptoms". National Institute on Aging. 2011-12-19. Retrieved 2011-12-19.

this:

• Alzheimer's Disease: Unraveling the Mystery. US Department of Health and Human Services, National Institute on Aging, NIH. 2008.

to this:

• Alzheimer's Disease: Unraveling the Mystery. US Department of Health and Human Services, National Institute on Aging, NIH. 2008.

and this:

• Caring for a Person with Alzheimer's Disease: Your Easy-to-Use Guide from the National Institute on Aging. US Department of Health and Human Services, National Institute on Aging, NIH. 2009.

to this:

• Caring for a Person with Alzheimer's Disease: Your Easy-to-Use Guide from the National Institute on Aging. US Department of Health and Human Services, National Institute on Aging, NIH. 2009.

There is also a citation that is currently not working that does not have a current live page; eventually, this content will be republished, so you may want to comment it out for now: "Can Alzheimer's disease be prevented" (PDF). National Institute on Aging. 2006-08-29. Retrieved 2008-02-29.

Thank you for your help in this matter. Please feel free to contact me if you have any questions about these requested changes.

-Max Handelsman MaxH (talk) 17:18, 27 December 2011 (UTC)

Done. You can reopen this request if you're still not autoconfirmed when "Can Alzheimer's disease be prevented" is republished by changing |answered= in the edit semi-protected template from "yes" to "no". Thanks for the update! — Bility (talk) 21:24, 28 December 2011 (UTC)

Problems with templates

The templates at the bottom aren't showing right, but I don't know what the problem is. I tried a couple of times to fix it, without luck, so I won't mess around with it any more. Lampman (talk) 16:24, 5 January 2012 (UTC)

This page is in Category:Pages where template include size is exceeded. You need to remove the template overload. DrKiernan (talk) 21:09, 10 January 2012 (UTC)

The html reads: <code><p><a href="/wiki/Template:CNS_diseases_of_the_nervous_system" title="Template:CNS diseases of the nervous system">Template:CNS diseases of the nervous system</a><!-- WARNING: template omitted, post-expand include size too large --> <a href="/wiki/Template:Amyloidosis" title="Template:Amyloidosis">Template:Amyloidosis</a><!-- WARNING: template omitted, post-expand include size too large --> <a href="/wiki/Template:Featured_article" title="Template:Featured article">Template:Featured article</a><!-- WARNING: template omitted, post-expand include size too large --><a href="/wiki/Template:Link_GA" title="Template:Link GA">Template:Link GA</a><!-- WARNING: template omitted, post-expand include size too large --> <a href="/wiki/Template:Link_GA" title="Template:Link GA">Template:Link GA</a><!-- WARNING: template omitted, post-expand include size too large --> <a href="/wiki/Template:Link_FA" title="Template:Link FA">Template:Link FA</a><!-- WARNING: template omitted, post-expand include size too large --></p> <!-- NewPP limit report Preprocessor node count: 235009/1000000 Post-expand include size: 2048000/2048000 bytes Template argument size: 779040/2048000 bytes Expensive parser function count: 11/500 --></code>

So the effect of maxing out the template post-expand include size is that these last few don't expand: {{CNS diseases of the nervous system}}, {{Amyloidosis}}, {{Featured_article}}, {{Link GA}}, and {{Link FA}}. The question really is "what template is causing the total to be so high, and what can we do about it?" LeadSongDog come howl! 06:50, 11 January 2012 (UTC)

The easiest solution is to remove one of either {{Mental and behavioral disorders}} or {{CNS diseases of the nervous system}}. If you want both, then you could try redesigning CNS diseases of the nervous system so that it uses hlist rather than template transclusion. I don't know if will work but it's the only idea I've got short of removing all the cite templates. DrKiernan (talk) 09:39, 11 January 2012 (UTC)

I tried that out, and removing {{CNS diseases of the nervous system}} squeeks it under the max, but the real problem lies earlier, and we'd likely just hit the max again for some other reason. I'll bet it's the massive number of citation templates, but I'm not eager to start chopping those down. LeadSongDog come howl! 15:47, 11 January 2012 (UTC)

On second look, perhaps it's a good thing. We've got an awful lot of refs cited here, many of which essentially say X was suggested (ref for X) but a subsequent review found no strong evidence for X (ref for not-X). We've also got a lot of pretty dated refs (we should probably not need many from earlier than Y2K) that could be replaced with a few Cochrane reviews. LeadSongDog come howl! 21:42, 11 January 2012 (UTC)

It may be worth emulating Talk:Autism/Archive_10#Page_loading_efficiency_and_style. The {{vcite}} template is said to generate smaller, faster-loading html than {{cite journal}}. If there's no objection, we could convert a few of the last refs to vcite and see what happens to the totals. LeadSongDog come howl! 14:36, 19 January 2012 (UTC)

I changed the cite journals to vcite journals, and I see the templates at the bottom now. DrKiernan (talk) 17:32, 19 January 2012 (UTC)

NYT: Path Is Found for the Spread of Alzheimer’s

• Path Is Found for the Spread of Alzheimer’s Ling.Nut3 (talk) 12:03, 3 February 2012 (UTC)

While interesting, it isn't a usable wp:MEDRS. It refers to this primary study and another, yet to be published in Neuron by BT Hyman et al. The comments on the first of these are also interesting reading. There likely will be a review discussing this soon, meanwhile there is wp:NODEADLINE. LeadSongDog come howl! 14:50, 3 February 2012 (UTC)

That's a pretty good summary of why I put it on Talk rather than in the article. ;-) Ling.Nut3 (talk) 16:41, 3 February 2012 (UTC)

Understood, but it needs to be repeated frequently to deter others from "helping" by working it into the article. ;-(

LeadSongDog come howl! 17:19, 3 February 2012 (UTC)

Edit request on 9 February 2012

A new pharmaceutical has been released

New FDA approved pharmaceutical food for treating Alzheimer's Disease

The brain typically uses glucose as its primary energy source. It is known that the ability to metabolize glucose is reduced in those suffering from Alzheimer’s disease. According to recent clinical data, ketone bodies can provide an alternative energy source as glucose metabolism becomes insufficient or unavailable. A new pharmaceutical food called AXONA has passed stage 1 clinical trials, where measurable improvement in cognitive function was demonstrated and has been approved for use by the FDA. The approach of Axona is to provide a source of Medium Chain Triglycerides (MCT) which the liver will convert to ketone bodies. These ketones can be utilized by brain cells as an alternative to the unavailable glucose. The MCT utilized by Axona is a C8 carbon chain known as Caprylic Acid, although in the powdered form used in Axona it is known as Caprylidene [C8]. Anecdotal evidence suggests that this same C8 carbon chain, caprylic acid which has been available from natural sources for some time in the form of coconut oil and MCT oil, may also be effective in the treatment of Alzheimer’s. Additional anecdotal evidence suggests that all MCT's, Caprylic Acid [C8], Capric Acid [C10],and Lauric Acid [C12] will be treated similarly by the liver, being converted to ketone bodies and made available to cells in need of an alternative energy source. It must be noted that there is currently no clinical data showing the effectiveness of any MCT other than that used in Axona. Axona®, MCT oil and coconut oil are similar in that their active ingredients for treating dementia are MCTs. At the same time, the types and mix of MCTs in each are different.

What Type of MCT is in Each Product?

	                                                 Three Products
                        Type of MCT	         Axona®	     MCT Oil	Coconut Oil
                      Caprylidene  [C8]	         47.5%	 	 
                     Caprylic Acid [C8]	 	              33%	    8%
                       Capric Acid [C10]	 	      67%	    7%
                       Lauric Acid [C12]	 	 	           48%

Total amount of the product made out of MCTs ( Axona® 47.50%) (MCT Oil 100%) (Coconut Oil 63%)

LINKS http://www.accerapharma.com/energymetabolism.html http://www.about-axona.com/pdf/prescribinginformation.pdf http://www.rose-hulman.edu/~brandt/Chem330/Ketone_bodies.pdf http://alzheimersweekly.com/content/axona-mct-coconut-oil-differences-benefits http://www.webmd.com/vitamins-supplements/ingredientmono-1138-LAURIC%20ACID.aspx?activeIngredientId=1138&activeIngredientName=LAURIC%20ACID

Video Links Dr. Newport's effective work on memory loss and Alzheimer's with coconut oil- Part I http://www.youtube.com/watch?v=iScs0uzQZFk&list=PL8AB3004B11E5C8F2&index=1&feature=plpp_video Dr. Newport's effective work on memory loss and Alzheimer's with coconut oil- Part II http://www.youtube.com/watch?v=LOrDIixbGMs&list=PL8AB3004B11E5C8F2&index=2&feature=plpp_video Dr. Newport's effective work on memory loss and Alzheimer's with coconut oil- Part III http://www.youtube.com/watch?v=fIfY-lHDLRk&feature=BFa&list=PL8AB3004B11E5C8F2&lf=plpp_video Dr. Newport's effective work on memory loss and Alzheimer's with coconut oil- Part IV http://www.youtube.com/watch?v=X2jp7BhDFrU&feature=BFa&list=PL8AB3004B11E5C8F2&lf=plpp_video Dr. Newport's effective work on memory loss and Alzheimer's with coconut oil- Part V http://www.youtube.com/watch?v=Up6JrQhaDUw&feature=BFa&list=PL8AB3004B11E5C8F2&lf=plpp_video Dr. Newport's effective work on memory loss and Alzheimer's with coconut oil- Part VI http://www.youtube.com/watch?v=G-IOs0JE1zg&feature=BFa&list=PL8AB3004B11E5C8F2&lf=plpp_video

Ejjr66 (talk) 23:31, 9 February 2012 (UTC)

None of those come even close to being a reliable source -- please read WP:MEDRS. Looie496 (talk) 00:22, 10 February 2012 (UTC)

Not done: As above and also reads like an advertisement. Sorry, Celestra (talk) 15:46, 10 February 2012 (UTC)