Identification of gene variants that affect the activity of neuronal sodium channels could help develop targeted therapies for patients suffering from excessive sweating.
Biomedical engineers at Duke University have developed an injectable biomaterial that helps transform the cavity left behind after a stroke caused by a blood clot into an environment more supportive of repair. By recruiting the body’s own immune cells, the treatment promoted the growth of new blood vessels, supported neural remodeling and improved motor performance in mice. The work appears in Cell Biomaterials.
Every year, millions of people experience strokes caused by blood clots, called ischemic strokes. Immediate treatments, including clot-dissolving drugs and mechanical removal of the clot, can restore blood flow and preserve threatened brain tissue. But these treatments cannot replace tissue that has already been lost.
Large strokes can result in substantial tissue loss and leave behind a cavity at the site of the injury. After the clot is removed, recovery relies largely on rehabilitation, which helps surviving brain circuits adapt but does not directly repair the damaged area.
This review by Graves et al. synthesizes emerging evidence that senescent brain cells are heterogeneous, dynamic, and context dependent, highlighting determinants of diverse programs and emphasizing integration of single-cell-and spatial-omics with mouse studies to facilitate mechanistic insights and possible therapeutics.
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In this episode of Lifespan, Dr. David Sinclair, A.O., Ph.D. – Professor of Genetics at Harvard Medical School and pioneer in longevity research – explores the science of eye aging, vision loss, and emerging strategies to preserve vision throughout life.
Dr. Sinclair shares an inside update on ER-100, including his team’s successful restoration of vision in non-human primates and the launch of the world’s first FDA-cleared age reversal human clinical trial. This Phase 1 clinical trial will evaluate the safety of epigenetic cellular restoration as a therapy.
Additionally, drawing on decades of research, Dr. Sinclair explains why the eyes may offer one of the earliest windows into biological aging, how everyday factors such as sleep position, alcohol consumption, and intraocular pressure influence long-term eye health, and what the latest evidence reveals about nutrition, supplements, and the connection between the eyes and the brain.
Take a blood sample from someone in the dead of winter. Take another in midsummer. Same person, same laboratory. And yet, at the level of gene activity, the molecular picture can look surprisingly different. This is not an anomaly. This, a new Nature Communications study argues, is simply how human biology works, and it has significant implications for the way biomarkers have traditionally been studied.
Researchers from Kiel University’s Excellence Cluster PMI, KU Leuven and the German Center for Neurodegenerative Diseases (DZNE) in Bonn tracked 333 volunteers in Flanders over six months, drawing blood three times and measuring the activity of roughly 14,000 genes on each occasion.
What they found suggests that an important source of biological variation has been underappreciated in many clinical studies: in 85% of all genes, the variation within a single person over time is larger than the variation between different people. In other words, for most genes, the largest differences are observed between two time points in the same individual rather than between different individuals.
Echolocation is a fascinating way that animals like bats and whales find their way around the world.
By emitting sounds and decoding the echoes that come back, these species are able to detect what’s around them in their local environment.
It’s something we know that humans can do too – and it takes less training than you might think.
Researchers identified two major intrinsic cardiac neuron populations in mice: Npy-positive neurons regulate parasympathetic heart rate control and support coronary perfusion, while Ddah1-positive neurons help maintain electrical stability during extreme stress. Removing Npy-positive neurons caused fatal cardiac failure, whereas loss of Ddah1-positive neurons increased susceptibility to malignant arrhythmias and sudden cardiac arrest under stress.