Talk:Biochemistry of Alzheimer's disease

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Biochemical Characteristics

The article states, "Levels of the neurotransmitter acetylcholine are reduced. Levels of the neurotransmitters serotonin, norepinephrine, and somatostatin are also often reduced. Glutamate levels are usually elevated." The article does not go into detail about what implications these changes could mean. Are these neurotransmitters, such as serotonin, only reduced in the affected areas of the brain? Are they reduced elsewhere in the body besides the brain? Does the increased Glutamate levels imply that there is too much Glutamate and therefore causes neuro-toxicity? — Preceding unsigned comment added by J.abraham.133 (talk • contribs) 00:30, 2 October 2014 (UTC)[reply]

New papers

Any use for this? Takashi Sakurai, Kumi Kaneko, Misako Okuno, Koji Wada, Taku Kashiyama, Hideaki Shimizu, Takumi Akagi, Tsutomu Hashikawa, and Nobuyuki Nukina (2008-10-20). "Membrane microdomain switching: a regulatory mechanism of amyloid precursor protein processing". The Journal of Cell Biology. 183 (2): 339–361. doi:10.1083/jcb.200804075. ISSN 0021-9525.{{cite journal}}: CS1 maint: multiple names: authors list (link) Related: PMID 18378702, PMID 17472586 Cheers,LeadSongDog (talk) 18:08, 20 October 2008 (UTC)[reply]

According to Physorg there's an interesting pathology paper in Science 3 April 2009 by Stuart A Lipton et al. If I get the drift, it says that nitric oxide from beta-amyloid promotes S-nitrosylation of the Drp1 protein, which is dimerized, then the dimers are involved in the causing fragmentation of mitochondria. The "multimers of beta-amyloid protein induce generation of nitric oxide, which reacts with Drp1 to cause excessive mitochondrial fragmentation and in turn neuronal damage." Sounds like it will be a very interesting read. LeadSongDog come howl 20:33, 2 April 2009 (UTC)[reply]

ADDLs??

I realize curing alzheimer's with olive oil is a figment of public relations press releases at this point, but I would like to have some bearings on "ADDLs" -- A[beta]-derived diffusible ligands, -- and how they relate to a-Beta and models of the pathophysiology of Alzheimers. Here are a couple of the links: [1] [2] It may just be a question of mentioning in the article (after some substances that are already mentioned there, maybe?) "also known as A[beta]-derived diffusible ligands or ADDLs" ... I had no idea from the first link above what on earth an ADDL was (they don't even bother to spell it out in the press release), and wikipedia let me down... cheers and thanks and keep up the great effortsCelia Kozlowski (talk) 22:48, 2 October 2009 (UTC)[reply]

Move to Pathophysiology of Alzheimer's disease

This is the WP:MEDMOS used term. Should we move it there?Doc James (talk · contribs · email) 04:03, 26 March 2011 (UTC)[reply]

U.S. Patent # 7858602

In U.S. Patent # 7858602----Rodriguez---Therapeutic and Prophylactic Uses of Cell Specific Carbonic Anhydrase in Treating Aging Disorders due to Oxidative Stress and as Growth Factors of Stem Cells The above discusses about the Pathophysiology and Treatment of almost all diseases of Mankind which includes Alzhimer's Disease Any use for this? {http://www.uspto.gov---U.S. Patent # 7858602--December, 28, 2010---Rodriguez````

Patents are not reliable sources. Please review WP:MEDRS.OrangeMarlin Talk• Contributions 17:03, 23 April 2011 (UTC)[reply]

Pathophysiology of Alzheimer's disease

Hi, Orangemarlin,

Reference Materials on the Pathophysiology of alzheimer's disease are all in U.S. Patent 7858602.

There are too manny references about alzheimer's disease.

How many references would you like me to give.

Will it be enough if I will just erase with reference to U.S. Patent # 7858602.

I am a Practicing Physician for 38 years.VRodrig110 (talk) 17:31, 23 April 2011 (UTC)[reply]

— Preceding unsigned comment added by VRodrig110 (talk • contribs) 17:24, 23 April 2011 (UTC)[reply]

VRodrig110 (talk) 17:29, 23 April 2011 (UTC)[reply]

Patents are not reliable sources. Patents aren't published in peer-reviewed journal, and no one in the patent office experimentally confirms or disputes it's finding. I'm not going to explain the legality of patents, because it is irrelevant. Second, your additions are nothing more than self-published writings. You should read WP:MEDMOS and WP:MEDRS. Finally, being a physician or not, or whether being one for 38 years or not, isn't what's important. OrangeMarlin Talk• Contributions 18:49, 23 April 2011 (UTC)[reply]

"Tau-ists" and "ba-ptists"

The article currently contains the following text:

The two positions are lightheartedly described as "ba-ptist" and "tau-ist" viewpoints in scientific publications by Alzheimer's disease researchers. "Tau-ists" believe that the tau protein abnormalities initiate the disease cascade, while "ba-ptists" believe that beta amyloid deposits are the causative factor in the disease.[18]

So one paper has made a religious pun. Does this really deserve to be restated in wikipedia? If so, the text should be modified to read:

The two positions are lightheartedly described as "ba-ptist" and "tau-ist" viewpoints in one scientific publication.[18]

Where I have outlined my suggested changes below.

The two positions are lightheartedly described as "ba-ptist" and "tau-ist" viewpoints in [one] scientific publication[remove "s"] [remove "by Alzheimer's disease researchers"]

If this change is rejected, then some additional evidence should be provided that this is a widely used phrase. Scientists often use puns and other ill-advised jokes in manuscript titles but that does not imply that these words are used int he scientific community. — Preceding unsigned comment added by 108.175.224.122 (talk) 02:50, 4 November 2012 (UTC)[reply]

Basically everyone thinks that both contribute. They are interrelated. Chamaemelum (talk) 00:26, 8 July 2023 (UTC)[reply]

AMPK and CAMKK2 Involved in the mechansims of Alzheimers disease

No mention of the role of AMPK in Alzheimers disease models (known since ~2009).
Could mention Team Unravels Central Mystery of Alzheimer's based on The CAMKK2-AMPK Kinase Pathway Mediates the Synaptotoxic Effects of Aβ Oligomers through Tau Phosphorylation.
Seems to be Amyloid beta oligmers activate CAMKK2 which activates AMPK which hyperphosphorylates tau (at S262) which causes loss of dendrites and synapses. - Rod57 (talk) 12:31, 12 April 2013 (UTC)[reply]

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duplications in text

mention of "tauopathy" occurs in two duplicates texts "AD is also considered a tauopathy due to abnormal aggregation of the tau protein" — Preceding unsigned comment added by MilanCela (talk • contribs) 08:18, 4 May 2017 (UTC)[reply]

Delete fringe

-Insulin signaling: fails Identifying reliable sources (medicine) page. Fringe. -Cholesterol hypothesis: fails Identifying reliable sources (medicine) page. Fringe. -Reelin hypothesis: should be deleted ASAP, worse than above two. If anything merge part of it into oxidative stress.

What do other people think? Which if any should be deleted (preferably), modified, or moved? Chamaemelum (talk) 00:25, 8 July 2023 (UTC)[reply]

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