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Parkinson's Involves Autoimmune Response to Alpha-synuclein

Wishful

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https://newatlas.com/medical/blood-analysis-signs-parkinsons-10-years/

I earlier posted speculation that a-syn is a possible factor in ME. Removal during sleep involves astrocytes, which might be malfunctioning due to ME. This latest report shows that a-syn binding to brain cells might make them targets for t-cells. The type of t-cell response changes over time (~ 10 years) from a strong response to an inhibiting response, then maybe no response.

I don't know whether this applies to ME, but it sounds like something that could be involved. Maybe we have higher levels of one form of a-syn (they vary in size and maybe binding sites) and our t-cells might respond differently to them, affecting brain function. Maybe a-syn binds to glial cells too, targetting them in an autoimmune response, messing up brain function.

A quick check turned up this paper: https://www.nature.com/articles/d41586-019-01832-0

It shows that interferon-gamma (which can be produced by t-cells, NK cells, and a few others) inhibits neural stem cells. Does anyone here know offhand whether a reduction in neural stem cells proliferation might cause some of ME's symptoms, such as brainfog?
 

pattismith

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It's interesting to notice that synucleinopathies (Parkinson Disease, Dementia with Lewis Body and Multi System Atrophy) involve alpha synuclein protein aggregates in
-neurons
-small nerve fibers
-glial cells (brain and spinal cords)

SFN is common in these diseases, and often showing up before brain symptoms.

This means that some serious diseases can affect both Brain + Small nerve fibers.

@Pyrrhus , you assume a common pathogenesis in small fibers and brain of ME patients. I understood your hypothesis is common infection in the brain and small fiber cells, am I right?
 

Pyrrhus

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Does anyone here know offhand whether a reduction in neural stem cells proliferation might cause some of ME's symptoms, such as brainfog?
I don't think anyone can answer that with any certainty. But there is a fascinating hypothesis that the symptom of depression is correlated with, and possibly caused by, a lack of neurogenesis in the hippocampus. Therefore, a reduction in neural stem cell proliferation may lead to the symptom of depression.
(Note that I am only referring to the symptom of depression, I am not referring to the diagnosis of depression, or any other definition of depression.)

@Pyrrhus , you assume a common pathogenesis in small fibers and brain of ME patients. I understood your hypothesis is common infection in the brain and small fiber cells, am I right?
I highly suspect a common pathogenesis in peripheral nerves and the brain of myself. I can't generalize the experiments I have conducted on myself to other people without conducting an appropriate clinical trial.

In my case, the evidence points to a persistent infection with Enterovirus A71. If you'd like to learn more about this, I am attaching the slides from a small talk I gave at Berkeley a few years back. (For privacy reasons, I have removed my name from the slides.)

Hope this helps.
 

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