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 of us? Data suggests it may be due to the telomere-shortening effect of current cancer treatments.
We knew animal germ cells undergo methylation changes to keep themselves young–and now we know that plants do too!
Stem cell exhaustion, one of the hallmarks of aging, seems to be partly regulated by another hallmark: nutrient sensing. Scientists just found that inhibiting mTOR with rapamycin leads to improved stem cell function in mice.
Are mutations within individual neurons a substantial source of aging damage? They’re certainly correlated, according to a recent study.
Stem cells prevent themselves from maturing out of pluripotency by modulating the rate of the DNA-unwinding process during cell division, and some researchers think this may be the key to creating more efficient reprogramming strategies.
File this under unintended consequences: cellular senescence evolved to prevent cancer, but by the end of life it’s doing more to help cancer.
Does aging proceed in the same sequence in all cells, or does each cell fail in its own unique way?
Once again, timely research on avoiding metabolic problems without having to forego your holiday feast: for mice, eating exactly twice a day without reducing overall calorie intake induces autophagy and causes fat loss.