autophagy

It's not really a foreign topic as there's 397 published papers on autophagy on PubMed.

So I don't know that there's any published link between excercise and neuronal autophagy.

This helps kick in autophagy [1], a process whereby our cells repair themselves; a garbage collector for our body if you will.

I wouldn't be surprised if the current research by that same lab was focusing on establishing a link to autophagy in neurons.

Does exercise induce autophagy in neurons?What are the most interesting developments in research?

I wonder if intermittent fasting would be an effective deterrent of ALS through autophagy, though I highly doubt this would be of much good after the disease takes hold.

I'm a bioinformatician, and I collaborated on an autophagy-related project a few years ago, so I had to read up on it then.

Upregulating autophagy by other means enhances life span.

These are how your skin knows to grow after an injury, how your immune system detects which cells are infected and need to be killed, and how your cells know which parts of themselves to digest via autophagy, among other things.

In fact pretty much everything that extends life in laboratory animals boosts autophagy one way or another - such as through altered expression levels of heat shock proteins and related regulators.

For example, autophagy is upregulated by calorie restriction.

I suspect that it's just the paper above showing a link between excercise and muscular autophagy, combined with the untested hypothesis of "Maybe excercise stimulates autophagy in other tisues too."

The plausible theory would be that increased autophagy cleans up damaged mitochondria, and mitochondrial function and damage are clearly very important determinants of longevity.

There is no concrete plan, nowhere near the level of understanding needed to even have a plan, and so people pick at proteins and mechanisms one by one that might be linked to calorie restriction or autophagy or other longevity-associated mechanisms.

"In the best scenario, five years of this will raise the water level enough for more meaningful approaches than calorie restriction mimetics, autophagy inducers, and other attempts at slow-aging drugs that have consumed billions to date with nothing to show for it, to raise significant funds themselves.

Nutrient signaling pathways involving growth hormone/insulin-like growth factor-1 axis and its downstream effectors, play a key role in DSR in response to starvation controlling the other cell maintenance systems, such as autophagy and apoptosis, that are related to the tumorigenesis.