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Microglia aging progresses through functional intermediate steps III

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE179698 | GEO | 2024/07/04

REPOSITORIES: GEO

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Microglia aging progresses through functional intermediate steps

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 | GSE179358 | GEO

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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.

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Puri2010 - Mathematical Modeling for the Pathogenesis of Alzheimer's Disease

Project description:Puri2010 - Mathematical Modeling for the Pathogenesis of Alzheimer's Disease Puri2010 - Mathematical Modeling for the Pathogenesis of Alzheimer's Disease Encoded non-curated model. Issues: - Confusing replacement of α16 when t = 3 years - Confusing 4th rate equation This model is described in the article: Mathematical modeling for the pathogenesis of Alzheimer's disease. Puri IK, Li L. PLoS ONE 2010; 5(12): e15176 Abstract: Despite extensive research, the pathogenesis of neurodegenerative Alzheimer's disease (AD) still eludes our comprehension. This is largely due to complex and dynamic cross-talks that occur among multiple cell types throughout the aging process. We present a mathematical model that helps define critical components of AD pathogenesis based on differential rate equations that represent the known cross-talks involving microglia, astroglia, neurons, and amyloid-? (A?). We demonstrate that the inflammatory activation of microglia serves as a key node for progressive neurodegeneration. Our analysis reveals that targeting microglia may hold potential promise in the prevention and treatment of AD. This model is hosted on BioModels Database and identified by: MODEL1409240001. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

2015-04-15 | MODEL1409240001 | BioModels

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

RNA-seq of lipid droplet-low and lipid droplet-rich microglia isolated from the hippocampi of LPS-treated young mice

Project description:Sequencing data related to the manuscript entitled, "Lipid droplet accumulating microglia represent a dysfunctional and pro-inflammatory state in the aging brain".

2019-11-06 | GSE139946 | GEO

RNA-seq of lipid droplet-low and lipid droplet-rich microglia isolated from the hippocampi of Progranulin KO mice

Project description:Sequencing data related to the manuscript entitled, "Lipid droplet accumulating microglia represent a dysfunctional and pro-inflammatory state in the aging brain".

2019-11-07 | GSE140009 | GEO

RNA-seq of lipid droplet-low and lipid droplet-rich microglia isolated from the hippocampi of aged mice

Project description:Sequencing data related to the manuscript entitled, "Lipid droplet accumulating microglia represent a dysfunctional and pro-inflammatory state in the aging brain".

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Project description:Attachment of human noroviruses to histo blood group antigens (HBGAs) is essential for infection, but how this binding event promotes the infection of host cells is unknown. Here, we employed protein NMR experiments supported by mass spectrometry and crystallography to study HBGA binding to the P domain of a prevalent virus strain (GII.4) in more detail . We report a highly selective transformation of N373, located in an antigenic loop adjoining the HBGA binding site, into an iso-aspartate residue. This spontaneous post-translational modification (PTM) proceeds with an estimated half-life of a few days at physiological temperatures, independent of the presence of HBGAs but dramatically affecting HBGA recognition.

2019-03-20 | PXD011914 | Pride

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