Targeting a metabolic interaction may offer a new route to clear senescent cells
Peer-Reviewed Publication
Updates every hour. Last Updated: 30-Oct-2026 20:15 ET (31-Oct-2026 00:15 GMT/UTC)
KYOTO, Japan, August 17, 2026 - Senescent cells - cells that have stopped dividing but remain metabolically active - can accumulate with age and contribute to chronic inflammation and tissue dysfunction. A new Mini Review in Geromedicine examines a protein interaction that may help some of these cells survive, highlighting a possible route toward more selective strategies for clearing them.
A therapeutic approach pioneered in Mainz for the treatment of multiple sclerosis (MS) is taking an important step toward clinical application. The team led by Professor Claire Jacob at Johannes Gutenberg University Mainz (JGU) is further developing a drug patch that could promote the repair of damaged myelin sheaths. ForTra gGmbH for Research Transfer (ForTra), a subsidiary of the Else Kröner-Fresenius Foundation, is supporting the project with EUR 1.1 million. The aim is to further develop the patch for production according to pharmaceutical quality standards and subsequently assess its safety and tolerability in an initial clinical trial.
Twin studies place the heritability of schizophrenia near eighty percent, but concordance between monozygotic twins falls well short of fifty percent. What occupies the remaining distance is unresolved. Consuelo Walss-Bass, who directs the Psychiatric Genetics Program and the brain collection at UTHealth Houston, approaches the problem through transcriptomic and epigenetic profiling of donated brain tissue and through induced pluripotent stem cell models derived from families with multiple affected siblings. She also grew up with the question: her mother had schizophrenia, and of five children raised afterward in Torreón, Mexico, one received the same diagnosis. Why My Sister? sets the two accounts alongside each other.
New research from the Marshall University Joan C. Edwards School of Medicine provides insight into how binge alcohol exposure during adolescence may cause lasting changes in brain function that persist into adulthood, potentially identifying a new target for future treatment approaches.
The study, published August 15 in Molecular Psychiatry, found that intermittent ethanol exposure during adolescence disrupted communication between astrocytes—supportive brain cells increasingly recognized for their role in neural signaling—and synapses in the hippocampus, a region of the brain important for learning and memory.