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- 1 Good summary article from New England Journal of Medicine (2004)
- 2 amyloid build up found in brains as young as 20 yo
- 3 Alois Alzheimer did not discover the disease
- 4 Aducanumab
- 5 "Study of thousands of brains reveals tau as driver of Alzheimer's disease", not amyloid
- 6 New Section under Cause: Sleep Disruption
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. Check date values in:
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?
- 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
- 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)
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)
"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."
"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.
Please add to the main article as you think appropriate.
- 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
- 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)