Project description:Our data demonstrate that genomic instability does not evidently contribute to naturally aging of the mouse heart and support the contention that the endogenous DNA repair machinery is remarkably active to maintain genomic integrity in cardiac cells throughout life.

2021-09-15 | GSE124005 | GEO

Genomic instability in the naturally and prematurely aged myocardium [variants: data set 2]

2021-09-15 | GSE129278 | GEO

Genomic instability in the naturally and prematurely aged myocardium [variants: data set 1]

2021-09-15 | GSE124083 | GEO

Genomic instability in the naturally and prematurely aged myocardium

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-09-15 | GSE124087 | GEO

Naturally-aged microglia exhibit phagocytic dysfunction accompanied by gene expression changes reflective of underlying neurologic disease

Project description:Age-associated microglial dysfunction contributes to the accumulation of amyloid-b (Ab) plaques in Alzheimer’s disease. Although several studies have shown age-related declines in the phagocytic capacity of myeloid cells, relatively few have examined phagocytosis of normally aged microglia. Furthermore, much of the existing data on aging microglial function have been generated in accelerated genetic models of Alzheimer’s disease. Here we found that naturally aged microglia phagocytosed less Ab over time. To gain a better understanding of such dysfunction, we assessed differences in gene expression between young and old microglia that either did or did not phagocytose Ab. Young microglia had both phagocytic and neuronal maintenance signatures indicative of normal microglial responses, whereas, old microglia, regardless of phagocytic status, exhibit signs of broad dysfunction reflective of underlying neurologic disease states. We also found downregulation of many phagocytic receptors on old microglia, including TREM2, an Ab phagocytic receptor. TREM2 protein expression was diminished in old microglia and loss of TREM2+ microglia was correlated with impaired Ab uptake, suggesting a mechanism for phagocytic dysfunction in old microglia. Combined, our work reveals that normally aged microglia have broad changes in gene expression, including defects in Ab phagocytosis that likely underlies the progression to neurologic disease.

2022-06-10 | GSE205803 | GEO

Multi-omic rejuvenation of naturally aged tissues by a single cycle of transient reprogramming

Project description:Multi-omic rejuvenation of naturally aged tissues by a single cycle of transient reprogramming

| PRJNA658337 | ENA

Multi-omic rejuvenation of naturally aged tissues by a single cycle of transient reprogramming [RRBS]

Project description:Multi-omic rejuvenation of naturally aged tissues by a single cycle of transient reprogramming [RRBS]

| PRJNA658342 | ENA