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| title = Alzheimer’s Disease: A Review |
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| year = 2018 |
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| author = Fymat, Alain L: International Institute of Medicine and Science |
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| url = https://scientiaricerca.com/srcons/pdf/SRCONS-02-00054.pdf |
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| org = Scientia Ricerca |
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==Wiki Education assignment: Perception== |
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== Good summary article from New England Journal of Medicine (2004) == |
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{{dashboard.wikiedu.org assignment | course = Misplaced Pages:Wiki_Ed/New_York_University/Perception_(Spring_2024) | assignments = ] | reviewers = ] | start_date = 2024-01-22 | end_date = 2024-05-11 }} |
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* {{cite journal |title=Alzheimer's Disease |
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|author=Cummings JL |
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|journal=N Engl J Med |date=2004 Jul |volume=351 |issue=1 |pages=56-67 |pmid=15229308 }} |
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== Aducanumab == |
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Results of a Phase II study of Aducanumab were released today. I think they are notable and well-covered by multiple secondary sources. Thoughts? --] ] 17:29, 20 March 2015 (UTC) |
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::Is there a review on the topic? ] (] · ] · ]) 23:37, 21 March 2015 (UTC) |
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== "Study of thousands of brains reveals tau as driver of Alzheimer's disease", not amyloid == |
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"By examining more than 3,600 postmortem brains, researchers at Mayo Clinic's campuses in Jacksonville, Florida, and Rochester, Minnesota, have found that the progression of dysfunctional tau protein drives the cognitive decline and memory loss seen in Alzheimer's disease. Amyloid, the other toxic protein that characterizes Alzheimer's, builds up as dementia progresses, but is not the primary culprit, they say. |
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The findings, published in ''Brain'', offer new and valuable information in the long and ongoing debate about the relative contribution of amyloid and tau to the development and progression of cognitive dysfunction in Alzheimer's, says the study's lead author, Melissa Murray, Ph.D., a neuroscientist at Mayo Clinic in Jacksonville. |
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The findings also suggest that halting toxic tau should be a new focus for Alzheimer's treatment, the researchers say." |
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<snip> |
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"Evidence suggests that abnormal tau then spreads from cell to cell, disseminating pathological tau in the brain's cortex. The cortex is the outer part of the brain that is involved in higher levels of thinking, planning, behavior and attention—mirroring later behavioral changes in Alzheimer's patients." |
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"Amyloid, on the other hand, starts accumulating in the outer parts of the cortex and then spreads down to the hippocampus and eventually to other areas," she says. "Our study shows that the accumulation of amyloid has a strong relationship with a decline in cognition. When you account for the severity of tau pathology, however, the relationship between amyloid and cognition disappears—which indicates tau is the driver of Alzheimer's," Dr. Murray says. |
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From: |
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http://medicalxpress.com/news/2015-03-thousands-brains-reveals-tau-driver.html |
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Please add to the main article as you think appropriate. |
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] (]) 18:26, 24 March 2015 (UTC) |
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:This debate has been going back and forth forever. We really need to wait until the findings are covered in reliable secondary sources before using them. An additional factor is that this new finding is not even being covered by the strongest popular science media, such as the New York Times, BBC, and Scientific American. It is only being covered by the plethora of science media that rely on press releases for their stories. When that happens, the chances are good that the story is not as significant as it may seem. ] (]) 20:09, 24 March 2015 (UTC) |
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::], where the research was published, is a professional, peer-reviewed journal published by Oxford U. Press. The research was not self-published. The research was, in fact, vetted by experts in the field prior to publication. NYT, BBC, SciAm: don't confuse popular media, even scientific popular media, with an Oxford U. professional peer-reviewed journal. They aren't even in the same league. BUT, for those who look to the MSM for scientifc/medical research, Bloomberg Business is now covering the story: http://www.bloomberg.com/news/articles/2015-03-24/alzheimer-s-debate-revived-even-as-biogen-s-drug-trial-advances |
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:::Do we have a high quality secondary source? ] (] · ] · ]) 09:49, 27 March 2015 (UTC) |
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:::Phantom, the rules that govern our use of sources are embodied in ]. Regarding the underlying problem here, rather than writing a long explanation let me refer you to a blog post I wrote last year, . The Bloomberg story is better than the others because it includes evaluations by independent experts -- but note that those experts are casting doubt on the significance of the study. ] (]) 14:32, 27 March 2015 (UTC) |
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==New Section under Cause: Sleep Disruption== |
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I am looking to make my first big edit to wikipedia. I would like to post a new section under causes entitled Sleep Disruption. Here is the bulk of that section. Please let me know if you have any suggestions before I attempt an edit to add this information. |
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A more recent explanation of Alzheimer's pathology postulates that sleep disruption can lead to or exacerbate already existing Alzheimer's Disease. Around 40% of Alzheimer's patients suffer from sleep disruption and it is the most common cause of institutionalization. In general, sleep fragmentation has been found to correlate with the incidence of the disease and there are various explanations for this hypothesis. |
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<span class="wikied-assignment" style="font-size:85%;">— Assignment last updated by ] (]) 03:49, 10 May 2024 (UTC)</span> |
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Slow wave sleep (SWS) is an important part of Non-rapid eye movement sleep that is implicated in facilitating memory consolidation. The amount of SWS is correlated with next day memory recall in healthy and Alzheimer's disease patients. (add additional source) During SWS, mammals express two well defined oscillatory patterns, hippocampal ripples and cortical spindles. In Alzheimer's disease, patients show a decrease in time spent in SWS and a decreased ratio of SWS to REM sleep. Patients also show a reduction in fast spindles and overall spindle density, two measures which are associated with accuracy on memory recall tasks. A reduction of SWS may lead to a breakdown of memory consolidation between the hippocampus and neocortex. |
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Hello! I previously edited this article for a course (also affiliated with Wiki Education) and have been keeping tabs on it as much as I could. At the time, I learned that we should avoid using documents such as the DSM to avoid copyright strikes. I noticed that after some edits to this article, the DSM itself is directly cited over a scientific review article discussing it (specifically in the Diagnosis (criteria) section). I wanted to ask about whether we could remove it, or if my understanding was incorrect. I am still learning so I hope this question isn't too bothersome! Thank you in advance! ] (]) 19:15, 15 August 2024 (UTC) |
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Sleep disruption also adds a new dimension to the Amyloid hypothesis. In healthy patients, Aβ levels increase with wakefulness, but decrease during rest. In patients with Alzheimer's disease, there is less variability in Aβ, which remains high at night. This correlates with sleep disruption and increased wakefulness, which may lead to an overall increase in Aβ production. Sleep disruption, therefore, could contribute to the build of Aβ proposed by the Amyloid hypothesis. |
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== Source - Life span == |
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Another possible cause of sleep disruption is deregulation of hypocretin, melanin-concentrating hormone (MCH) and melatonin, three neuropeptides important in sleep and wakefulness. A deficiency in hypocretin is associated with sleeping disorders such as narcolepsy. Patients with Alzheimer's have decreased levels of hypocretin and hypocretin-1 neurons. Low levels of hypocretin-1 has also been shown to correlate with increased sleep fragmentation in Alzheimer's. If hypocretin levels are deregulated in Alzheimer's disease, then this could lead to poor sleep quality and therefore increased memory impairment. |
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Broken link. ] (]) 23:31, 8 May 2024 (UTC) |
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MCH is correlated with Aβ levels and tau proteins associated with Alzheimer's. The levels of MCH in cerebral spinal fluid negatively correlate with memory. It has been suggested that misfolded tau protein tangles result in the hypersecretion of MCH, leading to daytime sleepiness and memory impairment. |
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:Thanks for reporting, I've fixed it by replacing the original reference with some newer and more precise ones. ] (]) 22:06, 9 May 2024 (UTC) |
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A potential treatment for Alzheimer's disease currently being tested is prolonged-release melatonin supplements. Melatonin improved sleep in Alzheimer's patients with and without insomnia, and it not only stopped memory decline, but improved performance after only 12 weeks. ] (]) 20:14, 11 April 2015 (UTC) |
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== "]" listed at ] == |
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::We need high quality secondary sources per ]. It is not clear your refs. Also please read ]. We tend to avoid words like "suffer" and write in a more encyclopedic tone. Best ] (] · ] · ]) 10:47, 12 April 2015 (UTC) |
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] |
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::: Agree with Doc ... please indicate your sources, and in addition to the pages above, review ] and ] (news). Unless you have secondary reviews mentioning these items, it sounds speculative. ] (]) 19:44, 14 April 2015 (UTC) |
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The redirect <span class="plainlinks"></span> has been listed at ] to determine whether its use and function meets the ]. Readers of this page are welcome to comment on this redirect at '''{{slink|Misplaced Pages:Redirects for discussion/Log/2024 May 21#Brain rot}}''' until a consensus is reached. <!-- Template:RFDNote --> ] (]) 23:27, 21 May 2024 (UTC) |
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== Amyloid beta theory under scrutiny == |
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== Life expectancy and prognosis in the Introduction == |
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Should the article be updated to reflect the doubts about the amyloid beta plaque theory? The paper on which that theory is based is under investigation for fraud now. Source: |
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''"Although the speed of progression can vary, the average life expectancy following diagnosis is three to nine years."'' |
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https://www.science.org/content/article/potential-fabrication-research-images-threatens-key-theory-alzheimers-disease ] (]) 19:32, 25 May 2024 (UTC) |
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:As described in ], the consensus seems to be that the alleged manipulation would not invalidate most of the research into the amyloid hypothesis. But since the report and the consequences have garnered significant attention from researchers as well as the general public, it would perhaps be a good improvement to mention it briefly in the ]. What do you think @]? (pinging you since you wrote most of the content covering this investigation). ] (]) 21:30, 2 June 2024 (UTC) |
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This needs to be improved upon in a few ways. First, the citations aren't the best - one has a data spread from 1990 to 2011 I think (too wide surely for a general "is" statement like this) while the other is not readable at all for me - not even a couple of lines (a link issue?) |
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::Thanks for the ping ... I agree with Bendeguz Acs that the sources indicate the alleged manipulation has little impact on most research, hence is not worthy of mention in the main article. As to whether it warrants a mention in the History section, my approach (particularly for a former ]) is to include only that which has been covered by secondary overall literature reviews -- the Lesne/Ashe issue has not risen to that level yet. Since this article has fallen from FA status, I won't strenuously object if it is added to History, but the standard I prefer is to base History on mention in overall literature reviews of the condition. ] (]) 15:37, 3 June 2024 (UTC) |
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'''Update''': {{u|Bendegúz Ács}} considering this (and the at ]), it seems there is some disagreement as to whether the findings cast doubt upon the prevailing amyloid hypothesis. Considering this is the most highly cited paper ever retracted, perhaps a one- or two- sentence summary at ] is warranted? I'm out of time for today, and although I did (partially) update Lesné, I haven't yet updated ], in case you have time to work there -- I am going to be fairly busy through Friday. Thanks for keeping up with this! I still don't find it necessary to make changes to this article, as we don't overplay the amyloid hypothesis here, and it is covered in detail at the Biochemistry of article. ] (]) 02:50, 5 June 2024 (UTC) |
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Background info: a number of people out there have survived this disease for 20 years now (since their first recorded signs - the person I care for has gone further and still lives at home with a full time carer and walks out daily, though language has almost gone down to a few single words like "thankyou" and the odd short habitual phrases interspersed with now-unrecognisable and mostly-meaningless gabble) -- and we know that the much shorter periods - like 2 or 3 years - can be linked to poor care. Certain care homes have little incentive to care beyond the time the average patient assets are depleted (ie around 3 years in the UK), while other establishments and many family carers go all out to make someone live as long as possible and can achieve stark differences. Care at its best is the most effective treatment of the disease, and has proved to be better that the drugs alone. In general, the better the general dementia care (which has improved over the years), the longer the patient lives. Care is of course linked to many things in dementia, which gradually increase as the suffer can does less - ranging from providing and monitoring diet to assuring continual hydration (which may not be mentioned enough in the article as it's the principle keyword in care) to simple attention, exercise, suitable activity and stimulus. I realise that all this has to be cited if included in the main page, but it still needs to be taken into consideration when structuring the other lines. |
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:I've also been busy, but I saw you made edits in both of those pages, I've reviewed them and they're great! I agree that ] is a good place to mention the retraction now. ] (]) 09:09, 8 June 2024 (UTC) |
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Also this detail on prognosis needs to be better/clearer on 'onset time' (which is hard to know of course) and 'diagnosis time' - which could be as any point down the line. Diagnosis of course gets better all the time. Currently we have very selective and out of date averages leading to a classic Misplaced Pages definitive (ie an x "is" y line). |
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==Wiki Education assignment: Human Anatomy Lecture== |
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If ever there was a detail to keep an eye on and attempt to improve upon, it is this one. It's barely changed in 10 years. I think in 2006 I edited this article a number of times, and wasn't that happy with whatever the figure was then. Remember that some people in referenceland have something akin to a vested interest in keeping the longevity figures down too: so the 3 year figure still gets touted a lot - far too much in my opinion as it represents a negative outlook. The person I mentioned about was given 6 months to get to the stage I described - now over 10 years ago. She was going down hill fast at the time, but her condition was actually reversed a degree and then drastically slowed. In the UK we are having a torrid time with various scandals on this issue - that of poor care basically. It skewers figures terribly. There is no money to be made in general public care. It's just an unfortuate reality I'm afraid - it all needs government subsidy really. The funding is never enough for the fully required level of care in all but the most select of care homes. With Alzheimer's you go down like a lead balloon without a sufficient level of care - it's terrifying to see how quickly people can drop (or be lifted a bit too if you are lucky - it can be very hard to see what's gone without taking the effort to look). Everytime I see a new and "existing" set of potential-treatment results ("ready within 10 years!"), it always strikes me how different the approach is to the last one I read. They just don't know enough about this disease I'm afraid. |
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{{dashboard.wikiedu.org assignment | course = Misplaced Pages:Wiki_Ed/University_of_Dayton/Human_Anatomy_Lecture_(Fall_2024) | assignments = ] | reviewers = ] | start_date = 2024-08-19 | end_date = 2024-12-06 }} |
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<span class="wikied-assignment" style="font-size:85%;">— Assignment last updated by ] (]) 04:30, 7 December 2024 (UTC)</span> |
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Anyway, a couple of tight lines need to be written that cover the past and the potentials re prognosis. I've had time to write this, but I'd appreciate it if someone else had a good look at it. ] (]) 03:32, 6 May 2015 (UTC) |
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Hello! I previously edited this article for a course (also affiliated with Wiki Education) and have been keeping tabs on it as much as I could. At the time, I learned that we should avoid using documents such as the DSM to avoid copyright strikes. I noticed that after some edits to this article, the DSM itself is directly cited over a scientific review article discussing it (specifically in the Diagnosis (criteria) section). I wanted to ask about whether we could remove it, or if my understanding was incorrect. I am still learning so I hope this question isn't too bothersome! Thank you in advance! Bharatss-SB (talk) 19:15, 15 August 2024 (UTC)
level-4 vital article is rated B-class on Misplaced Pages's content assessment scale.
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This article was the subject of a Wiki Education Foundation-supported course assignment, between 22 January 2024 and 11 May 2024. Further details are available on the course page. Student editor(s): Eg2619 (article contribs). Peer reviewers: PowdersPOWPOW.
The redirect Brain rot has been listed at redirects for discussion to determine whether its use and function meets the redirect guidelines. Readers of this page are welcome to comment on this redirect at Misplaced Pages:Redirects for discussion/Log/2024 May 21 § Brain rot until a consensus is reached. Based5290 (talk) 23:27, 21 May 2024 (UTC)