Trial Results for a PD-L1 Antibody Therapy to Reduce Inflammation in Alzheimer's Disease

A new study proposes a theoretical framework that explains why the more complex an animal is, the harder it is to move the needle on its rate of aging [1].

Mitochondrial transplantation is a promising approach to treating age-related mitochondrial dysfunction. Cells readily take up mitochondria from their surroundings.

The bacterial species P. gingivalis is a cause of periodontitis, a common form of inflammatory gum disease that in addition to damaging gums, teeth, and bone in the mouth, also contributes to the development of inflammatory age-related conditions elsewhere in the body.

Wang et al. identify TNFR1 signaling as a key link between inflammation and intestinal stem cell aging. This aging phenotype is transferable from old to young mice via shared circulation, suggesting systemic inflammation as a target to improve intestinal health.

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Social experiences and mortality risk: mediating roles of epigenetic aging, allostatic load, and health status

Frailty syndrome, characterized by diminished physiological reserves and heightened vulnerability to adverse health outcomes, is a major concern in aging populations.

Researchers at University of California San Diego and their colleagues have identified a key cellular pathway that drives brain degeneration in both a rare childhood disorder and the far more common Alzheimer's disease.

Microglia, the brain's resident macrophages, undergo metabolic reprogramming during aging, which impacts brain health and neurodegenerative disease risk.

The brain's immune cells are increasingly recognized as key players in Alzheimer's disease, but exactly how they change as the disease develops has remained unclear.