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(Medical Xpress)   "We don't think of Alzheimer's as fundamentally a disease of the brain. We think of it as a disease of the immune system within the brain"   (medicalxpress.com) divider line
    More: Interesting, Alzheimer's disease, Immune system, new mechanistic model, Neuron, Medicine, brain disease, beta-amyloid, most common form of dementia  
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406 clicks; posted to STEM » on 27 Sep 2022 at 3:53 PM (10 weeks ago)   |   Favorite    |   share:  Share on Twitter share via Email Share on Facebook



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2022-09-27 1:00:55 PM  
FTFA: The AD2 model endeavors to harmonize other mechanistic propositions (including proteopathy, synaptotoxicity and mitochondriopathy), while recognizing beta-amyloid as a physiologically oligomerizing immunopeptide and part of a much larger and broad, highly-interconnected immunopathic process. Within the AD2 model, amino acid metabolism of L-tryptophan and L-arginine emerge as innate immunity regulators.

Well geez, I could have told them that if they'd just asked.

/Mmmm, tryptophan...
 
2022-09-27 4:01:37 PM  
It would be interesting to see a genetic survey of people diagnosed with Alzheimer's and see if there is a correlation between any specific disease markers.

My mother has Alzheimer's and also has had active RA for 30-35 years.
 
2022-09-27 4:04:35 PM  
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2022-09-27 4:21:34 PM  
"It's definitely beta-amyloid this time guys, we swear"
 
2022-09-27 4:30:46 PM  

The Ocho: It would be interesting to see a genetic survey of people diagnosed with Alzheimer's and see if there is a correlation between any specific disease markers.

My mother has Alzheimer's and also has had active RA for 30-35 years.


"We can't possibly have 200 million respondents with Alzheimer's. How many people forgot and submitted multiple times!?"
 
2022-09-27 5:33:13 PM  
Is it lupus?
 
2022-09-27 5:38:28 PM  
So it IS lupu...

Dammit!
 
2022-09-27 7:15:24 PM  
dailydot.comView Full Size
 
2022-09-27 11:10:24 PM  
So at this point are we just intentionally looking away from the probability it's a prion disease because the prospect of an incurable, potentially contagious root cause is too terrifying to face?
 
2022-09-28 12:26:33 AM  
 
2022-09-28 12:31:15 AM  

The Ocho: It would be interesting to see a genetic survey of people diagnosed with Alzheimer's and see if there is a correlation between any specific disease markers.

My mother has Alzheimer's and also has had active RA for 30-35 years.


Processed foods such as refined fiberless carbohydrates can make RA flare

It has been proposed that the increase in ADs throughout Westernized societies over the last three decades could (at least in part) be explained by the increased intestinal permeability induced by industrial food additives
 
2022-09-28 1:20:27 AM  
Those Alzheimer's plaques are crusted in Complement neoantigen (basically polymerized activated Complement compounds and Membrane Attack Complexes in various stages of assembly).  Amyloid has been observed sprouting fibrils from areas of the SARS-CoV-2 spike protein that are the exact areas that trigger activation of Alternative Pathway of Complement.  Given the way Amyloid just soaks up those activated Complement compounds, I'm inclined to believe that Complement is much more indicated in the genesis and progression of Alzheimer's Disease than the current consensus interpretation supports.  Drugs that inhibit plaque formation don't slow down progression, and even exacerbate symptoms in about 40% of cases.

It's quite possible that the amyloid plaques are more symptom than cause.  Can't help but wonder if they change from benign to pathogenic configurations because they've been nuked to holy hell by the Complement System.

AD is one of those diseases that really deserves a first principles rework.  These models are built on assumptions that are 40 to 60 years old, and those assumptions--like Amyloid plaques being central to disease progression--may be overvalued, or even entirely incorrect.
 
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