Targeted Reduction of PTBP1 Reverses Cognitive Impairment in a Mouse Model of Alzheimer's Disease

Researchers here suggest that increased ERBB4 expression in neurons is an important driving mechanism in the onset and progression of Alzheimer's disease.

This is far from the only study to indicate that the children of long-lived individuals tend also to be long-lived. The open question is the degree to which this is genetic versus cultural transmission.

A substance found in edible sea squirts appeared to reverse several signs of aging in older mice. Plasmalogen supplements improved memory and learning, strengthened connections between brain cells, reduced inflammation, and even helped the mice grow thicker, darker hair.

Alzheimer’s disease (AD) is increasingly recognized as a neurodegenerative disorder associated with chronic low-grade inflammation and age-related immune dysregulation.

Language impairment is increasingly recognized as an early marker of neurodegeneration in mild cognitive impairment (MCI).

As aging populations drive rising global healthcare demands, finding scalable ways to prevent cognitive decline has become a vital public health priority.

Kidney aging is associated with increased proximal tubular senescence and leukocyte infiltration. Senolytic treatment reduces senescent cell burden and overall immune cell infiltration. However, macrophages remain enriched around residual senescent cells.

At the SENESCENCE2030 Annual Conference and Industry–Academia Workshop held in Coimbra, Portugal, in May 2026, researchers, clinicians, industry representatives and policy stakeholders identified the major priorities required to translate recent advances in cellular senescence research into clinical practice.

GLP-1 receptor agonism extends median lifespan in mice

Hutchinson-Gilford progeria syndrome (HGPS) is a premature aging disorder caused by a mutation in LMNA that produces the toxic progerin protein.