Researchers developed seven MRI-based biological age clocks across major organs using UK Biobank imaging, linking each to proteins, metabolites, genetics, disease risks, mortality, and cognitive decline. These organ-specific age gaps reveal how uneven aging shapes vulnerability to conditions such as diabetes, hypertension, and dementia, opening new paths for precision prevention and clinical trial stratification
Join us on Patreon! https://www.patreon.com/MichaelLustgartenPhD
Discount Links/Affiliates:
Blood testing (where I get the majority of my labs): https://www.ultalabtests.com/partners/michaellustgarten.
At-Home Metabolomics: https://www.iollo.com?ref=michael-lustgarten.
Use Code: CONQUERAGING At Checkout.
Clearly Filtered Water Filter: https://get.aspr.app/SHoPY
Epigenetic, Telomere Testing: https://trudiagnostic.com/?irclickid=U-s3Ii2r7xyIU-LSYLyQdQ6…M0&irgwc=1
Use Code: CONQUERAGING
NAD+ Quantification: https://www.jinfiniti.com/intracellular-nad-test/
October 21–22, 2025 (Online) 🌿
Dear colleagues and friends.
We are pleased to invite you to the International Scientific Conference “Anti-Aging: Science and Practice of Healthy Longevity”, organized by the Gerontology Section of the Moscow Society of Naturalists (MOIP) at Lomonosov Moscow State University, with the support of the Gerontology Society of the Ural Branch of the Russian Academy of Sciences (URAN).
📅 Dates: October 21–22, 2025 🕛 Time: 12:00–16:00 (Moscow time) 💻 Format: Online participation (free of charge) 🗣️ Working language: Russian.
🔹 October 21 — “Hypoxic Training (Therapy): Modern Aspects of Healthy Longevity Medicine” 🔹 October 22 — “Fundamental and Clinical Gerontology as the Basis of Healthy Longevity Medicine”
The conference will feature leading scientists from Russia, Germany, Belarus, Kyrgyzstan and other countries. Topics include: • Hypoxic therapy and adaptive mechanisms; • Geroprotection and the biology of aging; • Epigenetic reprogramming and cellular rejuvenation; • Applied aspects of active and healthy longevity.
🔗 Connection links: • Day 1 (October 21): https://my.mts-link.ru/j/38630705/5798697072
The gang catches up with Emil Kendziorra after the Biostasis 2025 conference at the European Biostasis Foundation. Watch it on YouTube here. Topics covered include:
• How to get a Tomorrow Bio ambulance in your hometown.
• Tomorrow Bio’s plan to collect brain samples to check ultra-structure preservation in its cryonics patients — and how it will respond to what it finds.
• What’s new and what’s next for Tomorrow Bio.
• Our near death experiences.
Links:
• Cryosphere Discord Server: / discord.
• Cryonics Subreddit: / cryonics.
In a study published in Neuron, a research team at the Department of Neurology at Massachusetts General Hospital, aimed to understand how immune cells of the brain, called microglia, contribute to Alzheimer’s disease (AD) pathology. It’s known that subtle changes, or mutations, in genes expressed in microglia are associated with an increased risk for developing late-onset AD.
The study focused on one such mutation in the microglial gene TREM2, an essential switch that activates microglia to clean up toxic amyloid plaques (abnormal protein deposits) that build up between nerve cells in the brain. This mutation, called T96K, is a “gain-of-function” mutation in TREM2, meaning it increases TREM2 activation and allows the gene to remain super active.
The researchers explored how this mutation impacts microglial function to increase risk for AD. The team generated a mutant mouse model carrying the mutation, which was bred with a mouse model of AD to have brain changes consistent with AD. They found that in female AD mice exclusively, the mutation strongly reduced the capability of microglia to respond to toxic amyloid plaques, making these cells less protective against brain aging.
face_with_colon_three Year 1998
In ancient Greece, immortality was the province of gods who spun the length of each lifetime. The myth has a kernel of truth, because the ends of chromosomes are protected by specialized stretches of DNA called telomeres. Once these are snipped too much by imperfect copying, a cell goes into senescence and stops dividing. Now two reports show that, with the help of an enzyme called telomerase, human cells can divide forever in the laboratory without turning cancerous. The findings, reported in the January issue of Nature Genetics, could ease the way to new treatments for burn victims, diabetics, and patients with other diseases.
Researchers hoped that adding telomerase would keep cells dividing long enough to replace tissues lost to injury or disease. Normal cells often have proved impractical because they can only divide a limited number of times in culture, and once returned to the body they’re often too old to do much good. The limitation may be that normal cells do not produce active telomerase, which can rebuild the telomeres and keep cells from becoming senescent.
In fact, about a year ago, Jerry Shay and his colleagues at the University of Texas Southwestern Medical Center in Dallas showed that adding the enzyme to normal connective tissue cells called fibroblasts extends their life-span (Science NOW, 13 January 1998). These cells have now lived three times longer than normal in the lab, and they are still going strong. But because cancer cells contain telomerase and also live forever, scientists worried that the newly immortal cells would become malignant when implanted in humans.
Women are far more likely than men to end up with Alzheimer’s disease (AD). This may, at least partially, be due to women’s longer average lifespans, but many scientists think there is probably more to the story. It would be easy to surmise that the increased risk is also related to differences in the way men’s and women’s brains change as they age. However, the research thus far has been unclear, as results across different brain regions and methods have been inconsistent.
Now, a new study, published in Proceedings of the National Academy of Sciences, indicates that it’s men who experience greater decline in more regions of the brain as they age. Researchers involved in the study analyzed 12,638 brain MRIs from 4,726 cognitively healthy participants (at least two scans per person) from the ages of 17–95 to find how age-related changes occurred and whether they differed between men and women.
The results showed that men experienced declines in cortical thickness and surface area in many regions of the brain and a decline in subcortical structures in older age. Meanwhile, women showed greater decline only in a few regions and more ventricular expansion in older adults. So, while differences in brain aging between the sexes are apparent, the cause of increased AD prevalence in women is still a bit mysterious.
