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This Organ Could Reverse Aging! Greg Fahy

If I had the money this would be the first person I would call.

Can one forgotten organ hold the key to reversing aging? In this exclusive interview, Dr. Greg Fahy — one of the world’s leading longevity scientists — reveals groundbreaking discoveries about the thymus, age reversal, and the future of human health.

From regrowing his own thymus to pioneering cryobiology and organ preservation, Dr. Fahy shares insights that could change how we think about aging, immortality, and life extension. This conversation dives into the science behind reversing biological age, restoring the immune system, and even the possibility of medical time travel.

🔑 Topics covered in this video:

Thymus regeneration and why it may be the “master control” of aging.

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How to stay young at DNA level? Harvard research finds surprising link between daily supplement and longevity

A Harvard-affiliated study suggests that daily vitamin D supplementation may help slow biological aging by protecting DNA and preserving telomere length. The VITAL trial, which tracked over 1,000 adults for four years, found that participants taking 2,000 IU of vitamin D daily experienced less telomere shortening, effectively reducing biological aging by nearly three years.

Why Do We Need Sleep? Oxford Scientists Trace the Answer to Mitochondria

Sleep may serve as more than rest for the mind; it may also function as essential upkeep for the body’s energy systems. A new study from University of Oxford researchers, published in Nature, shows that the drive to sleep is caused by electrical stress building up in the tiny energy-producing structures of brain cells.

This finding provides a concrete physical explanation for the biological need for sleep and has the potential to reshape scientific thinking about sleep, aging, and neurological disorders.

Switching Off One Crucial Protein Appears to Reverse Brain Aging in Mice

A protein called ferritin light chain 1 (FTL1) may play a significant role in brain aging, a new study reveals, giving scientists a new target for understanding and potentially preventing brain deterioration and disease.

FTL1 was brought to light through a careful comparison of the hippocampus part of the brain in mice of different ages. The hippocampus is involved in memory and learning, and it is one of the regions that suffers most from age-related decline.

The study team found that FLT1 was the one protein in this region that old mice had more of and young mice had less of.

Induced somatic mutation accumulation during skeletal muscle regeneration reduces muscle strength

With aging, somatic mutations accumulate in cellular DNA; however, whether they drive age-related functional decline is incompletely understood. Here the authors show that these mutations can weaken muscle repair and reduce strength after injury, suggesting they play a role in age-related physical decline in mouse muscle.

Microglia gene activity shifts across Alzheimer’s stages, revealing possible therapy targets

Alzheimer’s disease (AD) is a debilitating neurodegenerative disorder that causes progressive memory loss and a decline in mental (i.e., cognitive) abilities. Statistics suggest that between 500,000 and 900,000 people are diagnosed with this disease every year, while several hundreds of thousands experience dementia or other aging-related cognitive decline.

While there are some available treatments designed to delay cognitive decline in individuals with mild or moderate AD symptoms, a cure for the disease has not yet been identified. A better understanding of the neural, genetic, cellular and that contribute to the disease’s progression, as well as to neurodegeneration in general, could thus be highly valuable, as it could inform the future development of alternative treatments.

Past neuroscience research has identified the key role of microglia in AD. These are specialized that monitor the environment in the brain, clearing out , debris and pathogens. The dysregulation of these cells has been linked to neurodegeneration and to the progression of AD.

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