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Comment by omneity | Hacker News Reader

Can we possibly expect something similar for other neurodegenerative diseases such as Alzheimer's?

We have investigations into mitochondrial genetics and Alzheimer's. There's still a lot to learn but it's probably safe to assume there's a lot more going on. Treatment and even prevention for most will likely rely on attending to more than just mitochondrial abberations.

Physionic: Fasting and Overeating - How you Change your Mitochondria. [Study 32] https://www.youtube.com/watch?v=KQBmtzT4VTU Goes into great detail in how abundance of energy causes Mitochondrial to split into smaller pieces and go into high churn (low ATP output) but when in a low energy environment the Mitochondria join into longer chains and actually change how they work. There is other talks in how long chain Mitochondria outputs being used in brain cell inter communication and having said Mitochondria being too small massively inhibits those systems.

Mitochondria are at the center of a lot of key processes in general. They play an important role in regulating cell death and free radicals in the body. They also play a role that is still being studied in what membrane receptors are transported to the surface in neurons.

There's a lot that intersects at the mitochondria making it common across many pathogenesis and a very delicate system to interfere with (not ideal for intervention)

Crazy how important mitochondria are when you consider the evolutionary history.

Just so, so, so unlikely to happen to my small mind and stunning how far multicellular life has come with this symbiosis.

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