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Gas6 improves plaque burden, yet worsens behavior and induces microglial inflammation in the APP/PS1 model of Alzheimer’s disease

ABSTRACT: We sought to determine the effects of Gas6 on Alzheimer’s disease pathology through overexpression of Gas6 using an adeno-associated viral vector in the APP/PS1 model of Alzheimer’s disease. 9 month old male and female APP/PS1 and nontransgenic littermates received bilateral stereotactic hippocampal injections of AAV-Gas6 or AAV-control, an attenuated Gas6 protein that does not bind the Axl receptor. One month after injections, mice performed a battery of behavioral tasks and brains were processed for immunohistochemistry, transcriptional analyses, and flow cytometry.

ORGANISM(S): Mus musculus

PROVIDER: GSE171195 | GEO | 2022/03/30

REPOSITORIES: GEO

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Gas6 improves plaque burden, yet worsens behavior and induces microglial inflammation in the APP/PS1 model of Alzheimer’s disease

Project description:Gas6 improves plaque burden, yet worsens behavior and induces microglial inflammation in the APP/PS1 model of Alzheimer’s disease

| PRJNA718619 | ENA

Microglia use TAM receptors to detect and engulf amyloid beta plaques

Project description:Two microglial TAM receptor tyrosine kinases - Axl and Mer - have been linked to Alzheimer’s disease, but their roles in disease have not been tested experimentally. We find that in Alzheimer’s disease and its mouse models, induced expression of Axl and Mer in amyloid plaque-associated microglia is coupled to induced plaque decoration by the TAM ligand Gas6 and its co-ligand phosphatidylserine. In the APP/PS1 mouse model of Alzheimer’s disease, sIngle cell RNAseq analysis comparing wild type microglia with those with Axl and Mer deficiency reveals a similar disease state transitional program of microglia but a dampened differential expression of numerous AD siganture genes in microglia lacking TAM receptors. In line with the transcriptomic data, using two-photon microscopy, we show that genetic ablation of Axl and Mer results in microglia that are unable to normally detect, respond to, organize, or phagocytose amyloid beta plaques. These major deficits notwithstanding, and contrary to expectation, TAM-deficient APP/PS1 mice develop fewer dense-core plaques than APP/PS1 mice with normal microglia. Our findings reveal that the TAM system is an essential mediator of microglial recognition and engulfment of amyloid plaques, and that TAM-driven microglial phagocytosis does not constrain, but rather promotes, plaque development.

2021-02-25 | GSE160523 | GEO

Transcriptomic profile of FACS-isolated reactive or SOCS3-deactivated astrocytes from the hippocampus of wildtype and 9-month old APP/PS1dE9 mice

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Project description:Alzheimer’s disease (AD) is a progressive neurodegenerative disorder, and the molecular mechanisms of AD remain unclear. Accumulating evidence indicates the involvement of non-coding RNAs in AD pathogenesis. Here, we applied RNA-seq to explore the expression changes of circRNA, miRNA, and mRNA simultaneously, and investigate competing endogenous RNA (ceRNA) networks in hippocampus of 4-month APP/PS1 and wild-type mice.

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Expression data from WT mouse amd 9-month-old APP/PS1 mouse

Project description:To identify the differentially expressed genes in the brain of WT mice in comparison with 9-month-old APP/PS1 mice, we examined the microarray gene expression profile of the groups above. Neuroinflammation is well implicated in the progression of Alzheimer’s Disease (AD) now. What’ more, neuroinflammation is supposed to be one of the essential trigger to induce neurodegeneration. In this study, we examined the differentially expressed genes (including coding transcripts and lncRNA) between the wild type (WT) mouse and a AD model, the APP/PS1 mouse. We found that, among all these P2XR family genes, P2X7R is not only the most abundant expressed, but also identified as the highest upregulated gene. The elevated P2X7R expression promotes neuroinflammation through activation of NLRP3 inflammsome, and further mediate one kind of inflammatory cell death, pyroptosis. Blockade of P2X7R could not only inhibit pyroptosis, but also could mildly alleviate cognitive deficits in APP/PS1 mice. Our study provides new insight into an alternative strategy for the development of AD therapy.

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RNA-seq of frontal cortex in a novel mouse model of Alzheimer's disease.

Project description:There is accumulating evidence that amyloid beta and tau proteins may act synergistically to cause synapse and neural circuit degeneration in Alzheimer’s disease. In order to study this, we designed a new mouse model which lacks endogenous mouse tau, but expresses both the APP/PS1 transgene, which causes well-characterised plaque-associated synapse loss, and also reversibly expresses wild-type human tau (which can be suppressed with doxycycline). We examined the transcriptional changes in the frontal cortex of this mouse model, along with behaviour, pathology, synaptic plasticity, synapse degeneration and accumulation of amyloid beta and tau at synapses, and compared with littermate control genotypes: those lacking endogenous mouse tau, those lacking endogenous mouse tau but expressing the APP/PS1 transgene only, and those lacking endogenous mouse tau but reversibly expressing wild-type human tau only.

2019-11-12 | E-MTAB-7856 | biostudies-arrayexpress

Single-cell sequencing of endothelial cells of WT and APP/PS1 mice

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Project description:The assay for transposase-accessible chromatin by sequencing (ATAC-seq) was used to investigate the AD-associated chromatin reshaping in the APPswe/PS1dE9 (APP/PS1) mouse model. ATAC-seq data in the hippocampus of 8-month-old APP/PS1 mice were generated, and the relationship between chromatin accessibility and gene expression was analyzed in combination with RNA-sequencing.We identified 1690 increased AD-associated chromatin accessible regions in the hippocampal tissues of APP/PS1 mice and 1003 decreased chromatin accessible regions were considered to be related with declined AD-associated biological processes.In the APP/PS1 hippocampus, 1090 genes were found to be up-regulated and 1081 down-regulated. Interestingly, enhanced ATAC-seq signal was found in approximately 740 genes, with 43 exhibiting up-regulated mRNA levels.Our study reveals that alterations in chromatin accessibility may be an initial mechanism in AD pathogenesis.

2020-07-09 | GSE145907 | GEO

Characterization of the chromatin accessibility in an Alzheimer’s disease (AD) mouse model (ATAC-Seq)

2020-07-09 | GSE145906 | GEO

RNA-seq and TRAP-seq of astrocytes and brain tissue in mouse models of Alzheimer's pathology

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2021-12-02 | E-MTAB-10985 | biostudies-arrayexpress

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