Glucosamine: The new metformin? | Interview with Dr. Michael Ristow (part ii)

Last week when we heard from Dr. Ristow, he turned the outdated notion of the “free radical theory of aging” on its head, and demonstrated that antioxidants like vitamin A and vitamin C aren’t all they’re cracked up to be. But if those supplements can’t help us, what can? Perhaps, says Ristow, the answer can…

Research roundup: The naked (mole rat) truth, and more

What good is a longer life if you have to spend half of it keeping up with the news? Ditch those endlessly scrolling feeds, and instead join us every other week for a concentrated dose of the most exciting developments in the field of geroscience. Here’s the recap: Naked mole rats really do age better,…

Free radicals are not your enemy | An interview with Dr. Michael Ristow (part i)

Dr. Michael Ristow, a professor of energy metabolism at ETH Zurich, bases much of his research into aging on a premise that many of us will find surprising: the free radicals that our cells produce while making energy are not only not harmful, but can even slow the body’s aging down. But while that might…

Research roundup: Muscles from the lab, and more

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:…

Research roundup: The microbiome in neurodegenerative disease, and more

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.

Research roundup: The importance of energy in Alzheimer’s, and more

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

FOXO vs. a harbinger of neurodegeneration

Long before the usual physiological signs, the withering of neurons and the gradual atrophy of the brain, that tip doctors off to the presence of a neurodegenerative disease, there’s already something different about their patients’ brain cells. Action potentials flash across a long, thin arm protruding from the cell body in a healthy neuron, and…

Research roundup: Drifters in your epigenome, and more

Epigenetic markers “drift” as we age to cause unintended gene expression changes, but you might be able to slow this via caloric restriction. The epigenomes of rhesus monkeys on CR “appeared 7 years younger than their chronological age.” 7 years younger A vaccine for Alzheimer’s? It’s more likely than you think. Researchers at USC are…

Longevity orthologs: How far from the apple to the tree?

Laboratories studying the biology of aging are a menagerie of creatures great and small. From unicellular yeast and nematodes, all the way up to primates and even the faithful old Canis familiaris, animal models have opened up the aging process to our inspection in ways that human subjects wouldn’t have been able to match. It’s…

Research roundup: Scientists stop premature aging in its tracks, and more

Researchers from Houston Methodist Research Institute took cells from patients with progeria, a devastating condition that causes premature aging, and turned back the clock by lengthening their telomeres. Besides helping to cure a fatal disease, could these anti-aging benefits transfer to non-pathological aging? turned back the clock Men and women age differently–that’s no secret. But…

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