Postby Fiver » Mon Dec 09, 2019 7:16 am
Hi. Good questions!
Maybe this could help:
The mitochondria are indeed passed down from moms, except in very rare and extraordinary circumstances. But their circular chromosome is relatively small. Over the course of evolution many of the mitochondrial genes have been transferred from the mitochondria to the host cell's genome, making mitochondria dependent on the host cells. There are indeed some mitochondrial genes associated with disease, e.g., Leber Optical Blindness or the classic "mitochondrial diseases", but as far as I'm aware none of these are strongly and consistently associated with AD. I believe the classic risk genes are autosomal.
Mitochondrial dysfunction may be a component of AD - things like the production of harmful reactive oxygen by old or injured mitochondria, inhibition of the electron transport chain by toxins, or changes in how mitochondrial process different fuels (sugars vs. fats for example). This could be due to genetic factors or environmental factors.
One area of research aims to stimulate mitochondrial biogenesis (the production of new, healthy mitochondria to replace old, malfunctioning ones) with the goal of treating PD, MS, HD, DMD, AD, etc. Many of the lifestyle strategies and supplements discussed here seem to stimulate this, to some degree, in some cells, animals models, and maybe people.
I know less about a possible direct link between mitochondrial dysfunction of apoe4. I would have guessed the link would be indirect and related to the availability of various fuels and inflammation. Also, autophagy is the way old mitochondria are destroyed and recycled - so if that is disrupted it would make sense to have lots of poorly functioning mitochondria.
Thanks for this interesting thread!
Concerned, but hopeful. Introverted, but will talk about science.