We know you want to keep up with the relentless march of progress, but sometimes it’s just too relentless. So why not forget all those endlessly scrolling feeds, and instead join us for a bi-weekly concentrated dose of all the most exciting developments in the field of geroscience? Here’s what’s happened in the last two weeks:…

It’s looking increasingly likely that our little bacterial buddies have a major influence on neurodegenerative disease, from producing extra amyloid, to regulating inflammation, to generating free radicals. In mouse models of Alzheimer’s disease, a protein complex that forms part of the nervous system’s innate immune system binds to toxic amyloid-beta, promoting the formation of plaques.

Since the world of Alzheimer’s therapeutics hasn’t seen much practical benefit from targeting harmful proteins like amyloid-beta, maybe other approaches like targeting dysfunctional mitochondria are worth exploring in more depth. Apparently, improving mitochondrial function can decrease plaque burden and improve cognition in a mouse model. Why do cancer survivors have shorter lifespans than the rest

It looks like those clumps of tau protein that form inside the neurons of Alzheimer’s brains may actually be protective, and the real damage might instead come from tau oligomers. If you take a major flesh wound to the emergency room for treatment, they probably won’t slather a metformin cream on you… but maybe they…

Keeping one eye on your calories, and the other on that delicious-looking pumpkin pie? Don’t worry–your Thanksgiving sins probably won’t hurt your longevity as long as you’re fasting sometimes. You can thank your gut bacteria. What do insulin resistance and 17th century Prague have in common? The first rare variant that dramatically increases human lifespan…

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