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:
For the first time ever, scientists have transformed a totally different tissue (skin, in this case) into genuine muscle fibers that can contract and respond to external stimuli. How did they succeed where other attempts failed? They grew their reprogrammed cells in a 3D matrix.
A blood-sugar controlling drug originally developed for diabetes may be able to treat Alzheimer’s, according to results from mouse studies.
Normally, cancers defy the daily rhythms controlling nutrient supply to cells. So what happens if you limit their supply by forcing them to obey the circadian clock? Smaller, less aggressive tumors, naturally.
For all of you drinkers out there, a team at Cambridge just watched the toxic byproduct that your body produces when it processes alcohol do its work on the DNA of mice. What they found were broken strands that made the mice more prone to mutations and ultimately cancer. Great conversation starter at parties!
In biomarker news, Insilico has used its ample data resources to develop a model that can predict mortality in multiple genetically distant populations.
A drug derived from the spice curcumin becomes the newest link between Alzheimer’s treatment and treatment for other aging diseases. Researchers working on bringing the drug to clinical trials for Alzheimer’s have found that its mechanism of action has to do with ATP synthase, a precursor to ATP and a general modulator of aging in animal models.
Here’s an unusual argument for the “mutation accumulation” theory of aging: mutant cells are especially prone to propagating daughter cells (which would carry the same mutations), even when they’re not actually cancerous.
Can old, dysfunctional stem cells be saved from exhaustion in old age by the signals of young cells?
Senolytics are only supposed to remove senescent cells, so you might have a problem if yours kills normal cells as well–as the senolytic quercetin apparently does.
Young brains use glial cells to help prune unwanted connections between neurons, while in adulthood they keep synapses in good order. But in a surprising twist, these cells revert back to youthful pruning behavior in old age, especially in the brain regions most vulnerable to aging. This may explain why older neurons are so hard of hearing: their support cells have essentially “cut the phone lines”.