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→‎Causation (answered): NYU source is dated and not a valid source
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:::Alzheimer's Association ref. added. -- [[User:Jo3sampl|Jo3sampl]] ([[User talk:Jo3sampl|talk]]) 16:17, 1 October 2011 (UTC)
:::Alzheimer's Association ref. added. -- [[User:Jo3sampl|Jo3sampl]] ([[User talk: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::I agree that the source is out of date.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. [[User:Presto54|Presto54]] ([[User talk:Presto54|talk]]) 07:39, 13 October 2011 (UTC)


== Edit request from Feelsky, 2 October 2011 ==
== Edit request from Feelsky, 2 October 2011 ==

Revision as of 07:39, 13 October 2011

Featured articleAlzheimer'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 Wikipedia community. Even so, if you can update or improve it, please do so.
Main Page trophyThis article appeared on Wikipedia's Main Page as Today's featured article on September 21, 2008.
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October 14, 2006Peer reviewReviewed
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August 25, 2008Featured article candidatePromoted
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Correlation to (particularly midlife) diabetes

See PMID 18952836 18952836 for details.

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)


References

Please keep this section at the end of the talk page.

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)[reply]

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)[reply]

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)[reply]

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)[reply]

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)[reply]

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 (talkcontribs) 22:07, 30 September 2011 (UTC)[reply]
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)[reply]
Alzheimer's Association ref. added. -- Jo3sampl (talk) 16:17, 1 October 2011 (UTC)[reply]
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)[reply]

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)[reply]
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)[reply]

Edit request from , 12 October 2011

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)[reply]

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)[reply]