Aging rhesus macaques display distinct fluid proteomic signatures of senescence and neuropathology
Plasma proteins tracked aging and amyloid pathology more closely than cerebrospinal fluid across the non-human primate lifespan.
21 results
Plasma proteins tracked aging and amyloid pathology more closely than cerebrospinal fluid across the non-human primate lifespan.
The compound lowered senescence markers and improved heart function through SIRT3-driven DRP1 deacetylation in aged mice and cultured cardiomyocytes.
Large human cohort data and cell experiments show that ASXL1-driven clonal hematopoiesis worsens aortic valve hemodynamics and promotes calcification through inflammatory signaling.
Oral treatment restored bone density and mechanical strength while suppressing inflammatory markers and rebalancing intestinal bacteria in a disuse model.
Dysregulated phospholipid and bile acid metabolism tracked with cytokine spikes and 180-day mortality, while a specific lipid attenuated senescent markers in cell tests.
Exposure to environmental arsenic caused heart dysfunction via the p53 and p21 pathway, which quercetin treatment reversed in cultured rat cardiomyoblasts.
Clustering four age-associated inflammatory cytokines separated adults into three distinct endotypes tied to early chronic lung disease risk.
The culture platform maintained native tissue architecture for four weeks, revealing treatment effects on aged donor tissue that emerged only after prolonged exposure.
The treatment reduced oxidative stress, suppressed inflammation, and remodeled the gut microbiome in naturally aging mice while prolonging survival in nematodes.
Single-cell profiling reveals distinct neutrophil subsets that promote senescence in vascular and liver cells while altering bone marrow progenitor states.