This is an excellent comment, and I’m very glad to see my thinking inspiring others!
My own findings on the issue are as such:
I am confident that mitochondrial dysfunction is upstream of AD.
This one gene called PGC 1 alpha is probably involved or something.
I do not know what (if anything) is upstream of that. It could be immune system health but the immune system is so complex that my understanding of it is generally poor.
Mitochondria which are defective are replaced in cells through a process called mitophagy. Stimulating the creation of mitochondria (mitogenesis) probably increases mitophagy too as cells can regulate themselves pretty well.
Drugs which stimulate mitophagy and mitogenesis are probably more productive avenues for AD research than lots of things, an example of each is metformin and EET-A respectively. EET-A has an effect on amyloid plaques in mice but that isn’t that useful (however I think that information is worth more when a mechanistic story can be told).
I suspect that AD is an “attractive state” that brains just fall into for lots of reasons, this explains the endless feedback loops confusing researchers, and also it being much more common than lots of other brain diseases.
AD is an interesting microcosm of not just brain health, but also of ageing in general. An effective anti-ageing therapy would almost certainly eliminate AD or at least stop progression. An effective AD therapy is worth investigating as a general anti-ageing therapy (although if it’s that effective on ageing we’ll probably notice).
This is an excellent comment, and I’m very glad to see my thinking inspiring others!
My own findings on the issue are as such:
I am confident that mitochondrial dysfunction is upstream of AD.
This one gene called PGC 1 alpha is probably involved or something.
I do not know what (if anything) is upstream of that. It could be immune system health but the immune system is so complex that my understanding of it is generally poor.
Mitochondria which are defective are replaced in cells through a process called mitophagy. Stimulating the creation of mitochondria (mitogenesis) probably increases mitophagy too as cells can regulate themselves pretty well.
Drugs which stimulate mitophagy and mitogenesis are probably more productive avenues for AD research than lots of things, an example of each is metformin and EET-A respectively. EET-A has an effect on amyloid plaques in mice but that isn’t that useful (however I think that information is worth more when a mechanistic story can be told).
I suspect that AD is an “attractive state” that brains just fall into for lots of reasons, this explains the endless feedback loops confusing researchers, and also it being much more common than lots of other brain diseases.
AD is an interesting microcosm of not just brain health, but also of ageing in general. An effective anti-ageing therapy would almost certainly eliminate AD or at least stop progression. An effective AD therapy is worth investigating as a general anti-ageing therapy (although if it’s that effective on ageing we’ll probably notice).