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Gene expression profile of ACSA-2+/O1-/CD11b-/Cd45-/Olig4- astrocytes from the brain V

ABSTRACT: We used bulk RNA sequencing to investigate the molecular signature of astrocytes affected by microglial APOE4 in P301S mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE234485 | GEO | 2023/07/31

REPOSITORIES: GEO

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Gene expression profile of ACSA-2+/O1-/CD11b-/Cd45-/Olig4- astrocytes from the brain I

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Gene expression profile of ACSA-2+/O1-/CD11b-/Cd45-/Olig4- astrocytes from the brain IV

Project description:Gene expression profile of ACSA-2+/O1-/CD11b-/Cd45-/Olig4- astrocytes from the brain IV

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Gene expression profile of ACSA-2+/O1-/CD11b-/Cd45-/Olig4- astrocytes from the brain V

Project description:Gene expression profile of ACSA-2+/O1-/CD11b-/Cd45-/Olig4- astrocytes from the brain V

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Project description:Gene expression profile of ACSA-2+/O1-/CD11b-/Cd45-/Olig4- astrocytes from the brain II

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Gene expression profile of ACSA-2+/O1-/CD11b-/Cd45-/Olig4- astrocytes from the brain I

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Complement C1q-dependent synapse elimination by astrocytes in a mouse model of Alzheimer's disease

Project description:Synapse loss and glial activation are hallmarks of Alzheimer's disease (AD). In Tau P301S transgenic mice, the complement pathway contributes to neuronal damage through microglial elimination of synapses. Here, we used unbiased proteomic profiling of postsynaptic density (PSD) fractions from Tau P301S mice in C1q-WT versus C1q knockout backgrounds to identify C1q-dependent changes at synapses. Integrative multi-omics analysis revealed that astrocyte- and microglia- specific proteins are increased in Tau P301S synapse fractions with age and in a C1q-dependent manner. The same set of glial proteins (including C1q, C4, Gpnmb, and S100a4) is elevated in human AD synaptic fractions, and C4 levels are raised in cerebrospinal fluid (CSF) from AD patients. Besides microglia, we show that astrocytes contribute substantially to excitatory and inhibitory synapse engulfment in Tau P301S hippocampus. Based on staining of synapse markers within lysosomes, astrocytes showed preference for excitatory synapses whereas microglia preferred to engulf inhibitory synapse markers. Genetic deletion of C1q reduced astrocytic eating of excitatory and inhibitory synapses in Tau P301S mice, and rescued synapse density. Together, our data indicate that astrocytes contact and phagocytose synapses in a C1q- dependent manner and thereby contribute to synapse loss and neurodegeneration in AD.

2021-11-03 | MSV000088313 | MassIVE

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