Talk:Tauopathy
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The contents of the Argyrophilic grain disease page were merged into Tauopathy on November 2010. For the contribution history and old versions of the redirected page, please see its history; for the discussion at that location, see its talk page. |
Wiki Education Foundation-supported course assignment
editThis article is or was the subject of a Wiki Education Foundation-supported course assignment. Further details are available on the course page. Student editor(s): Msmarelli.
Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 10:44, 17 January 2022 (UTC)
Over Enthusiastic
editThis page is not of encyclopedia standard . It is too one sided and does not mention the other school of thought on Alzheimers. I am agnostic on this one. BillO'Slatter (talk) 03:00, 1 August 2008 (UTC)
- Perhaps a little harsh, but yes, I'd have liked to see more about β-amyloid plaque formation (to be fair, that, if it's associated with the pathology of Alzheimer's Disease, it's only tangentially so. Clinical trials of verubecestat, which blocks β-secretase demonstrated no benefit to patients at all). loupgarous (talk) 21:53, 16 December 2017 (UTC)
Life and Death in Assisted Living
editFrontline (U.S. TV series) will be running Life and Death in Assisted Living on Tuesday July 30th: http://www.pbs.org/wgbh/pages/frontline/pressroom/frontline-propublica-investigate-assisted-living-in-america/ Please contribute to discussion Talk:Assisted_living#Life_and_Death_in_Assisted_Living XOttawahitech (talk) 03:47, 30 July 2013 (UTC)
Article Critique
editContent
The article does not seem to have an overall focus and could be better organized. Following the short leading section, there are two extremely short paragraphs that are related to another and should be combined into one larger paragraph. After those two paragraphs, statements related to tauopathies are essentially listed with no order and these statements are not organized into distinct sections. Due to the little detail that is given, the presentation is a bit hard to understand. The article is short and is more of a partial overview of the topic. The protein tau should be discussed more in detail, such as mentioning that there are six isoforms of tau and which isoforms are implicated in Alzheimer's disease. Also, more attention should be given to the alternate hypothesis of Alzheimer's disease, the beta-amyloid hypothesis
I am only familiar with tauopathy in its relation to Alzheimer's disease; the evidence in the article pertaining to AD appears to be accurate to my knowledge, though there should be more information given about the disease. Some of the statements made are not cited, such as some of the diseases listed as primary tauopathies. The citation in the Huntington's disease paragraph does not follow the same format as the other citations. The content could be improved, as stated above by adding more information about the protein tau, covering the alternate Alzheimer's disease hypothesis, adding references to the statements that lack them, adding more useful and well-labelled diagrams, and explaining some of the concepts in greater detail, such as an explanation of what a 4R/3R balance is.
Quality
The article has a short introduction, which is mostly understandable. There is one phrase that references "the disease" but there was no indication of what this disease was. This introduction did not summarize the key points of the article. There are no headings or subheadings present in the article. There is some important content missing as noted above. Also, there could be more images/diagrams present in the article, such as a diagram of the mechanism of one of the primary tauopathies. The diagram that is there is at an appropriate place in the article. The coverage is a bit biased towards the tau hypothesis in Alzheimer's disease, briefly mentioning the beta-amyloid hypothesis. No facts in particular are emphasized. Most of the references seemed reliable, though the article referenced one particular journal, Acta Neuropathologica multiple times, which could indicate possible bias. One of the journals claimed that articles would be guaranteed to be published within ten days, which seems a bit rushed.ms277614 (talk) 15:13, 6 March 2018 (UTC)
Content
editTwo issues here - sourcing first.
Sourcing The initial version of this was obviously copy/pasted from somewhere, with no attribution in the edit note, which is not OK.
The second version had sources that were way too old and were primary.
The third version (below) has one recent review which is better. Frontiers Media is a near-predatory publisher and I generally avoid it, but it is at least a recent review. But this still has old, and primary sources. Unclear why this is being insisted on.
The second issue is that this is WP:OFFTOPIC as it stands. We already have an article - an FA at that, on Alzheimer's disease and another on Alzheimer's disease research. It is unclear how this is meant to fit into this topic or where this is going and how it is meant to knit with the rest of the encyclopedia....
- Beta-amyloid ===
Extracellular senile plaques comprised of beta-amyloid (Aβ) are present in Alzheimer’s disease and precede neurofibrillary tangle formation.[1][2] Aβ is derived from the amyloid precursor protein (APP); enzymes β-secretase and γ-secretase cleave APP to form Aβ peptides, which are then secreted from the neuron.[3] Once secreted, Aβ peptides can aggregate, which eventually forms the plaques in Alzheimer’s disease. Mutations in APP and presenilin genes are observed in early-onset Familial Alzheimer’s Disease (FAD).[4]
References
- ^ Hardy, J. A.; Higgins, G. A. (1992-04-10). "Alzheimer's disease: the amyloid cascade hypothesis". Science (New York, N.Y.). 256 (5054): 184–185. ISSN 0036-8075. PMID 1566067.
- ^ Kametani, Fuyuki; Hasegawa, Masato (2018). "Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease". Frontiers in Neuroscience. 12: 25. doi:10.3389/fnins.2018.00025. ISSN 1662-4548. PMC 5797629. PMID 29440986.
{{cite journal}}
: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link) - ^ Hardy, John; Selkoe, Dennis J. (2002-07-19). "The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics". Science (New York, N.Y.). 297 (5580): 353–356. doi:10.1126/science.1072994. ISSN 1095-9203. PMID 12130773.
- ^ Murrell, J.; Farlow, M.; Ghetti, B.; Benson, M. D. (1991-10-04). "A mutation in the amyloid precursor protein associated with hereditary Alzheimer's disease". Science (New York, N.Y.). 254 (5028): 97–99. ISSN 0036-8075. PMID 1925564.
Tau tangles Predictive of Alzheimer brain lesions
editAlzheimer 'tau' protein far surpasses amyloid in predicting toll on brain tissue(and its ref) suggest tau tangle locations predict future brain lesions associated with Alzheimers. Uses investigational flortaucipir to image tau tangles in a PET scan. Could mention somehow. - Rod57 (talk) 11:15, 4 January 2020 (UTC)