A new longevity breakthrough could change how scientists think about aging.
This discussion explores why discoveries like these could reshape the future of healthy aging.
This clip is from the following episode: • Mira Murati’s 975B Open Model, Ramin Hasan…
Recorded on July 16, 2026
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The brain’s immune system has long been thought to exist independently from the rest of the body, complete with its own specialized immune cells and a blood-brain barrier that limits what can travel into the brain.
Now, Stanford researchers have found that aging brings with it a large influx of immune cells into the brain, a discovery that not only upends current thinking but could also open new avenues for treating neurological disease. The researchers describe their results in the journal Nature.
“We usually think of the brain as a closed system,” said Julia Belk, a postdoctoral scholar in pathology at Stanford Medicine and first author on the new study. “What we found is that actually a lot of immune cells enter the human brain during aging.”
Telomere shortening is associated with increased risk of disease and decreased lifespan. Various nutrients have been shown to support the length and health of telomeres in clinical and preclinical studies.
Scientifically reviewed by: Gary Gonzalez, MD, in May 2026. Written by: Richard Ross.
In 2015, Liz Parrish flew to Colombia and let someone inject an untested gene therapy into her body 150 times. She texted her kids that she loved them before it started. When it was over, she went for nachos.
Ten years later, her telomeres are longer than when she started, and she has taken 12 gene therapies in total.
Her decade of self-experimentation has produced peer-reviewed data, a growing protocol of gene therapies, and a company training its sights on making biological aging optional. Our conversation goes over what it took to become patient zero and what gene therapy for aging looks like in practice today, among other things.
et al. used an innovative series of screening and directed evolution steps to produce a new enzyme (CMLase) which can remove a pernicious form of advanced glycation end product (AGE) linkage from proteins. AGEs contribute to biological aging, so CMLase may possess therapeutic potential to combat parts of the aging process.
Advanced glycation end products (AGEs) in proteins, a hallmark of aging, are considered irreversible. Here, authors report the development of CMLase — an enzyme that specifically oxidizes Nε-carboxymethyl-lysine (CML) and restores the native lysine residues in vitro and in human tissue samples.
A review finds that restricting protein, particularly methionine, isoleucine, and valine, may improve metabolism and influence key aging pathways, largely in experimental models. Short human studies suggest metabolic benefits, but effects on lifespan remain unknown and restriction may harm people with unmet or increased protein needs.
Cells must constantly repair damage to their DNA that, if left unfixed, can lead to cell death, cancer, or accelerated ageing. EMBL researchers and their collaborators show that the Golgi complex, an organelle best known as the cell’s sorting and shipping centre, stores DNA-repair proteins and dispatches them to the nucleus when damage occurs. When DNA is damaged, the cell recruits the relevant repair proteins from the Golgi to the nucleus, matched to the type of damage, and clears the proteins it doesn’t need out of the nucleus, sequestering them back at the Golgi. This work reveals a new layer of regulation of DNA repair pathways from outside the nucleus, opening up new opportunities to modulate these pathways and to target related diseases such as cancer.