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Transcriptional profiling of microglia in the injured brain reveals distinct molecular features underlying neurodegeneration

ABSTRACT: Transcriptional profiling of microglia in the injured brain reveals distinct molecular features underlying neurodegeneration

PROVIDER: PRJNA687185 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13288437_1.fastq.gz	Fastqsanger.gz
	SRR13288437_2.fastq.gz	Fastqsanger.gz
	SRR13288438_1.fastq.gz	Fastqsanger.gz
	SRR13288438_2.fastq.gz	Fastqsanger.gz
	SRR13288439_1.fastq.gz	Fastqsanger.gz

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Transcriptional profiling of microglia in the injured brain reveals distinct molecular features underlying neurodegeneration

Project description:We applied whole transcriptome analysis of microglia acutely isolated at different timepoints after a cortical stab wound injury to gain insight into genes that might be dysregulated and transcriptionally different between males and females after cortical injury.

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Temporal tracking of microglia activation in neurodegeneration at single-cell resolution

Project description:In this study, we used single-cell RNA-sequencing to gain unprecedented insight into the phenotypic heterogeneity and the transcriptional dynamics of microglia cells during the progression of neurodegeneration. Briefly, by using a severe neurodegeneration mouse model with Alzheimer’s-like pathology and phenotypes (CK-p25 model), we surveyed microglia activation by RNA sequencing longitudinally at fine temporal- and single-cell resolution. In summary, our work identified previously unobserved heterogeneity in the response of microglia to neurodegeneration, discovered novel microglia cell states, revealed the trajectory of cellular reprogramming of microglia in response to neurodegeneration, and uncovered the underlying transcriptional programs. These insights into the molecular programs underlying microglia activation provided by our study may pave the way for designing new rational and efficient strategies to treat Alzheimer’s and other neurodegenerative diseases.

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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

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Transcriptional Profile of Microglia in Neurodegeneration

Project description:Purpose: RNASeq was used to identify transcriptional signature responsible for the metabolic reprogramming phenotype of microglia in neurodegenerative disease Result: We identified Ppargc1a/Cebpb signaling pathway as a critical axis that controls microglial glycolytic transition during neurodegeneration

2020-08-28 | GSE92550 | GEO

RNA-seq analysis of microglia and infiltrating macrophages in the injured retina

Project description:The goal of this study is to identify genes differentially expressed between microglia and infiltrating macrophages in the injured retina Methods: mRNA profiles of microglia (Cont) and infiltrating macrophages (GFP) at day 7 post-injry, quadruplicated, were generated by deep-sequencing using Illumina HiSeq 2500 sequencer. Results: RNA-seq tags were mapped to the mouse mm9 reference genome assembly using Tophat2 ver. 2.0.8b, with FPKM values caluculated with Cufflinks ver. 2.1.1 with the default option.Comparison of gene expression between microglia and infiltrating macrophages identified genes specific to each subset. Conclusions: Our study provides the detailed analysis of transcriptomes in microglia and infiltrating macrophages in the injured retina

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Unique microglia recovery population revealed by single-cell RNAseq following neurodegeneration

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Microglia-mediated T cell Infiltration Drives Neurodegeneration in Tauopathy

Project description:Extracellular amyloid-β (Aβ) deposition as neuritic plaques and intracellular accumulation of hyperphosphorylated, aggregated tau as neurofibrillary tangles (NFT) are two of the characteristic hallmarks in Alzheimer’s disease (AD). The regional progression of brain atrophy in AD highly correlates with tau accumulation but not amyloid deposition and the mechanisms of tau-mediated neurodegeneration remain elusive. Innate immune responses represent a common pathway for the initiation and progression of some neurodegenerative diseases. To date, little is known about the extent or role of the adaptive immune response in the presence of Aβ or tau pathology. We systematically compared the immunological milieus in the brain of mice with amyloid deposition or tau aggregation and neurodegeneration. We found that mice with tauopathy but not amyloid, developed a unique innate and adaptive immune response and that depletion of microglia or T-cells blocked tau-mediated neurodegeneration. T cells, especially cytotoxic T cells, were markedly increased in areas with tau pathology in mice with tauopathy and in the AD brain. T cell numbers correlated with the extent of neuronal loss, and dynamically transformed their cellular characteristics from activated to exhausted states along with unique TCR clonal expansion. Inhibition of IFN-γ and PD-1signaling both significantly ameliorated brain atrophy. Our results thus reveal a tauopathy and neurodegeneration-related immune hub involving activated microglia and T cell responses, which could serve as therapeutic targets for preventing neurodegeneration in AD and primary tauopathies.

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Microglia-mediated T cell Infiltration Drives Neurodegeneration in Tauopathy

Project description:Microglia-mediated T cell Infiltration Drives Neurodegeneration in Tauopathy

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