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	Alzheimer's disease is a featured article; it (or a previous version of it) has been identified as one of the best articles produced by the Misplaced Pages community. Even so, if you can update or improve it, please do so.
	This article appeared on Misplaced Pages's Main Page as Today's featured article on September 21, 2008.
Article milestones Date Process Result July 3, 2006 Good article nominee Listed October 14, 2006 Peer review Reviewed June 12, 2008 Featured article candidate Not promoted August 25, 2008 Featured article candidate Promoted A news item involving this article was featured on Misplaced Pages's Main Page in the "In the news" column on August 10, 2010. Current status: Featured article

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Ideal sources for Misplaced Pages's health content are defined in the guideline Misplaced Pages:Identifying reliable sources (medicine) and are typically review articles. Here are links to possibly useful sources of information about Alzheimer's disease. PubMed provides review articles from the past five years (limit to free review articles) The TRIP database provides clinical publications about evidence-based medicine. Other potential sources include: Centre for Reviews and Dissemination and CDC

This article is written in British English, which has its own spelling conventions (colour, travelled, centre, defence, artefact, analyse) and some terms that are used in it may be different or absent from other varieties of English. According to the relevant style guide, this should not be changed without broad consensus.

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

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

amyloid build up found in brains as young as 20 yo

Here's a couple of links to news articles re. finding amyloid build up in brains of people as young as 20 y.o. Could a regular editor add this info to the AD article?

http://www.dailymail.co.uk/health/article-2975071/Early-signs-Alzheimer-s-disease-patients-young-20-Unprecedented-findings-say-disease-eats-away-cells-50-years-symptoms-develop.html

https://www.yahoo.com/health/early-signs-of-alzheimers-disease-found-in-112519622602.html

Phantom in ca (talk) 22:49, 3 March 2015 (UTC)

We would need a medical review to add/cite this material; it's a bit premature anyway - the referenced primary source/study (apparently published March 2nd in a journal titled "Brain") isn't pubmed indexed as of writing this. Seppi333 (Insert 2¢ | Maintained) 00:44, 4 March 2015 (UTC)

Alois Alzheimer did not discover the disease

http://genome.wellcome.ac.uk/doc_WTD020951.html Alois Alzheimer did not discover the disease nor did he claim to.--Wool Bridge (talk) 21:18, 4 March 2015 (UTC)

Ref says "In 1907, using the Bielschowsky stain on the case that made him famous, Alois Alzheimer described a startling new pathology in the brain of a recently deceased woman who died a few years after developing a clinically unusual dementia at age 51. The novel neuropathological feature that Alzheimer observed consisted of tangles of fibrils within the cyptoplasm of neurons, which were stained in sharp definition by the silver impregnation. His description included the following excerpt:" Doc James (talk · contribs · email) 22:36, 4 March 2015 (UTC)

Was that wellcome trust piece published? Doc James (talk · contribs · email) 22:38, 4 March 2015 (UTC)

Aducanumab

Results of a Phase II study of Aducanumab were released today. I think they are notable and well-covered by multiple secondary sources. Thoughts? --Walter Siegmund (talk) 17:29, 20 March 2015 (UTC)

Is there a review on the topic? Doc James (talk · contribs · email) 23:37, 21 March 2015 (UTC)

"Study of thousands of brains reveals tau as driver of Alzheimer's disease", not amyloid

"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.

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.

The findings also suggest that halting toxic tau should be a new focus for Alzheimer's treatment, the researchers say."

<snip>

"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."

"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.

From: http://medicalxpress.com/news/2015-03-thousands-brains-reveals-tau-driver.html

Please add to the main article as you think appropriate.

Phantom in ca (talk) 18:26, 24 March 2015 (UTC)

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. Looie496 (talk) 20:09, 24 March 2015 (UTC)

Brain_(journal), 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

Do we have a high quality secondary source? Doc James (talk · contribs · email) 09:49, 27 March 2015 (UTC)

Phantom, the rules that govern our use of sources are embodied in WP:MEDRS. Regarding the underlying problem here, rather than writing a long explanation let me refer you to a blog post I wrote last year, The trouble with press release-based science reporting. 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. Looie496 (talk) 14:32, 27 March 2015 (UTC)

New Section under Cause: Sleep Disruption

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.

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.

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.

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.

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.

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.

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. KimonoKagaku (talk) 20:14, 11 April 2015 (UTC)

We need high quality secondary sources per WP:MEDRS. It is not clear your refs. Also please read WP:MEDMOS. We tend to avoid words like "suffer" and write in a more encyclopedic tone. Best Doc James (talk · contribs · email) 10:47, 12 April 2015 (UTC)

Agree with Doc ... please indicate your sources, and in addition to the pages above, review WP:RECENTISM and WP:NOT (news). Unless you have secondary reviews mentioning these items, it sounds speculative. SandyGeorgia (Talk) 19:44, 14 April 2015 (UTC)

Life expectancy and prognosis in the Introduction

"Although the speed of progression can vary, the average life expectancy following diagnosis is three to nine years."

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 (a ink issue?)

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.

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).

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.

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. Matt Lewis (talk) 03:32, 6 May 2015 (UTC)

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