Project description:Aged microglia contribute to maladaptive inflammation, but little is known about their progression from homeostasis to dysfunction during aging. Here, we analyze the spatiotemporal kinetics of microglial aging in the hippocampus. Spatially, the dynamics of age-related inflammatory changes in microglia vastly differ across adjoining regions. Using single cell RNA-Sequencing and in vitro approaches, we find that microglia aging proceeds progressively through functional intermediate states that are necessary for inflammatory activation.

2024-07-04 | GSE190007 | GEO

Microglia aging progresses through functional intermediate steps

2024-07-04 | GSE179358 | GEO

Microglia aging progresses through functional intermediate steps III

2024-07-04 | GSE179698 | GEO

Microglia aging progresses through functional intermediate steps II

2024-07-04 | GSE179611 | GEO

Microglia aging advances through intermediate states that drive inflammatory activation and cognitive decline

Project description:TGFB-signaling is important for the establishment of microglia homeostasis; however, it's role in aging has remained vague. We found that Tgfb1 and TGFB signaling is altered during hippocampal microglia aging. To investigate the effects that microglia-derived Tgfb1 has on microglia aging, we performed scRNA-Seq on Cd11b+ cells from the hippocampus of mature mice where Tgfb1 had been ablated from Cx3cr1 cells post-maturity.

2024-07-04 | GSE211340 | GEO

Microglia aging advances through intermediate states that drive inflammatory activation and cognitive decline

Project description:Microglia aging advances through intermediate states that drive inflammatory activation and cognitive decline

| PRJNA869921 | ENA

SIRT1 deficiency in microglia contributes to cognitive decline in aging and neurodegeneration via epigenetic regulation of IL-1beta

Project description:Aging is the predominant risk factor for neurodegenerative diseases. One key phenotype as brain ages is the aberrant innate immune response characterized by proinflammation. However, the molecular mechanisms underlying aging-associated proinflammation are poorly defined. Whether chronic inflammation plays a causal role in cognitive decline in aging and neurodegeneration has not been established. Here we established a mechanistic link between chronic inflammation and aging microglia, and demonstrated a causal role of aging microglia in neurodegenerative cognitive deficits. Expression of microglial SIRT1 reduces with the aging of microglia. Genetic reduction of microglial SIRT1 elevates IL-1Î² selectively, and exacerbates cognitive deficits in aging and in transgenic mouse models of frontotemporal dementia (FTD). Interestingly, the selective activation of IL-1Î² transcription by SIRT1 deficiency is likely mediated through hypomethylating the proximal promoter of IL-1Î². Consistent with our findings in mice, selective hypomethylation of IL-1Î² at two CpG sites are found in normal aging humans and demented patients with tauopathy. Our findings reveal a novel epigenetic mechanism in aging microglia that contributes to cognitive deficits in neurodegenerative diseases. Study of changes related to alterations of SIRT1 levels in microglia of young and aged animals and in models of neurodegenerative dementia

2014-10-01 | E-GEOD-56452 | biostudies-arrayexpress

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