Comment by bransonf | Hacker News Reader

Comment by bransonf | Hacker News Reader

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Of the research I’ve read, many scientists suggest that it’s the accumulation of plaques that cause Alzheimer’s.[0]

There’s uncertainty as to what protein is responsible for the degenerative effects.[1]

My bias exists for the fact that I believe the cure to Alzheimer’s is removing or preventing the development of this plaque. At least I’ve been lead to believe this is among the most promising cures.[2] Amyloid protein is particularly tricky because it’s insoluble. I don’t think we could develop a purely chemical solution for the fact that it would likely be destructive to our own biology. And I think both gene expression and enzyme production are unlikely to be able to changed with just a drug.

[0] https://www.sciencedaily.com/releases/2018/03/180326161000.h...

[1] https://www.sciencemag.org/news/2016/05/tau-protein-not-amyl...

[2] https://rupress.org/jem/article/215/3/927/42616/BACE1-deleti...

See this case of a Colombian woman whose brain is full of the amyloid plaque but she is demntia free due to a genetic mutation

https://www.sciencemag.org/news/2019/11/colombian-woman-s-ge...

The beta amyloid theory is pretty tired at this point since the correlation between plaques and Alzheimer's is only moderate.

Imo Alzheimer's is probably more related to the brain falling into dysdunctional, self reinforcing patterns of synaptic connectivity.

Neural plaques might exacerbate this problem by disrupting connectivity, but clearly the brains of many people with plaques learn to route around this damage to retain functionality.

> self reinforcing patterns of synaptic connectivity

Any sources for this? I’d be very interested to read the literature on this.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4207354/

Just a jumping off point review on the weakness of the amyloid theory.

The connectome dysregulation theory is my own, it hasn't appeared in the scientific literature as of yet due to our inability to perform fine mapping of synaptic connections without microtoming a cadaver brain.

That's a cool theory. The brain tries pretty hard to maintain criticality (hard as in, disruptions cause it to return to that setpoint quickly). It's possible that inability to recover or maintain optimal processing criticality can lead to corruption of the connectome.

https://www.sciencedaily.com/releases/2019/10/191007113314.h...

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