Talk:Alzheimer's disease
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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.
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References
Please keep this section at the end of the talk page.
Hello, Would like to see some changes in this article regarding the following sentence:
"Because AD cannot be cured and is degenerative, the sufferer relies on others for assistance."
This is no more true, AD could be treated successful with Cannabis:
Marijuana linked to preventing and treating Alzheimer's disease Alzheimer's disease is the leading cause of dementia among the elderly, and with the ever-increasing size of this population, cases of Alzheimer's disease are expected to triple over the next 50 years. Consequently, the development of treatments that slow or halt the disease progression have become imperative to both improve the quality of life for patients as well as reduce the health care costs attributable to Alzheimer's disease. Here, we demonstrate that the active component of marijuana, Δ9-tetrahydrocannabinol (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid β-peptide (Aβ) aggregation, the key pathological marker of Alzheimer's disease. Computational modeling of the THC-AChE interaction revealed that THC binds in the peripheral anionic site of AChE, the critical region involved in amyloidgenesis.
Compared to currently approved drugs prescribed for the treatment of Alzheimer's disease, THC is a considerably superior inhibitor of Aβ aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease.
Edit request from , 12 October 2011
{{edit semi-protected}} 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)
- 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)
- That's not written at a level that is appropriate for this article, regardless of whether better sources come along. This top-importance and very widely read article must try to stay accessible to a broad range of readers. Looie496 (talk) 15:13, 13 October 2011 (UTC)
- Per the above comment, and WP:RECENT, and Wikipedia:Make technical articles understandable, this request is declined for now. If there is consensus here for the request, please use a further {{edit semi-protected}}. Chzz ► 00:04, 14 October 2011 (UTC)
Prion research on Alzheimer's
Prions may cause Alzheimer's. Could someone add something on this. http://www.nature.com/news/2009/090225/full/news.2009.121.html --Ericg33 (talk) 01:45, 2 November 2011 (UTC)
- The paper in question only gives evidence that prion proteins play a role in Alzheimers, not that they cause it. In any case that's a primary research article and therefore not a good source for us to use. However it has been very widely cited, and is discussed in at least two reviews, including PMID 20698011 and this paper from PubMed Central. Looie496 (talk) 02:19, 2 November 2011 (UTC)
Also known as
Alzheimer's disease (AD), also called Alzheimer disease, senile dementia of the Alzheimer type, primary degenerative dementia of the Alzheimer's type, simply Alzheimer's (as a stand-alone attributive adjective noun), and folk-etymological names such as "old-timers' disease", is the most common form of dementia is an awfully long sentence, especially considering there are only six words of fact in it! Do we really need all of those aka's, all but one of them with "Alzheimer" in them, in the first sentence? If it was also commonly known as "Joe Bloggs' disease" or "brain-rot" it would be worth including aka's so that readers would know they were on the page they were looking for, but as it is the reader is thoroughly befuddled before he or she gets to the all-important "...is the most common form of dementia." Why not a separate "Name" section if all of those variants are worth mentioning? 86.41.20.6 (talk) 11:17, 15 November 2011 (UTC)
- I agree. Moved the names; separate section might be better. -- Jo3sampl (talk) 02:18, 17 November 2011 (UTC)
- I have created a separate section for reasons apparent when you read it. The two modern terms, Alzheimer's disease and Alzheimer disease, are equivalent and almost equally common in the literature, like Parkinson's disease and Parkinson disease. Both should be left in the lede as it would be a big fight to figure out which to drop. The article could be renamed also, but the same applies. SBHarris 02:37, 17 November 2011 (UTC)
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