How Senescence Spreads Between Brain Cells

Rehabilitation following a stroke that causes significant loss of function is a slow, painful, and uncertain process. The concept underlying these efforts is that the brain will attempt to rebuild neural connections given sufficient efforts to use lost and diminished function.

Cells become senescent constantly throughout life, in response to damage, stress, or reaching the Hayflick limit on replication. A senescent cell ceases to replicate, grows in size, and begins to secrete a potent mix of pro-inflammatory signals.

First generation stem cell therapies that use a variety of cell sources and protocols are widely used in the medical tourism industry. A more limited set of such therapies are used in more regulated medical systems.

ANGPTL8 increases with age in humans and mice and serves as a key predictor of biological aging and mortality. Adipocyte-derived ANGPTL8 promotes cellular senescence through AKT2–mTOR signaling, whereas genetic deletion of Angptl8 attenuates adipose tissue aging and extends lifespan.

Association of data-driven dietary patterns with arterial stiffness: a cross-sectional study of 1155 Chinese adults

“What I finally decided was the organizing principle was that psychiatry aims at reduction of symptoms, but not restoration of the full human experience that makes life most worthwhile.”‒ Linus Abrams

A research team led by Professor Keisuke Goda of the SiRIUS Institute of Medical Research and Graduate School of Medicine at Tohoku University, together with the Department of Chemistry at the University of Tokyo, has been named a Milestone 2 Awardee of…

An experimental Alzheimer’s compound prevented damaging protein clumps from forming in the brains of mice, helping nerve cells survive longer and reducing amyloid buildup.