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Gene expression changes associated with Alexander disease (AxD)

ABSTRACT: Gene expression changes associated with Alexander disease (AxD)

PROVIDER: PRJNA478185 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7441430.fastq.gz	Fastqsanger.gz
	SRR7441431.fastq.gz	Fastqsanger.gz
	SRR7441432.fastq.gz	Fastqsanger.gz
	SRR7441433.fastq.gz	Fastqsanger.gz
	SRR7441434.fastq.gz	Fastqsanger.gz

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Genetic modifiers of GFAP expression in mouse models of Alexander disease

Project description:Gene expression analysis was performed in mouse models with Alexander disease associated GFAP mutations

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Gene expression changes associated with Alexander disease (AxD)

Project description:We use human induced pluripotent stem cell (hiPSC)-derived astrocytes and post-mortem human brain tissues to study gene expression changes associated with AxD

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Microglia sense astrocyte dysfunction and prevent disease progression in an Alexander disease model

Project description:Alexander disease is a neurodegenerative diseases caused by mutations of GFAP, an astrocyte-specific gene. We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of astrocytes.

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Hippocampal gene expression in the GFAP-R237H rat model of Alexander disease at early and late stages of disease

Project description:Alexander disease is a rare neurodegenerative disorder caused by mutations in the gene for glial fibrillary acidic protein (GFAP), the major intermediate filament of astrocytes in the central nervous system. GFAP mutation causes a toxic gain-of-function and protein aggregation, ultimately leading to gliosis, astrocyte dysfunction, and neurodegeneration. To better understand the disease process, a rat model has been generated to mimic the common R239H mutation observed in the human disease (R237H in the rat). This study focuses on hippocampus, a brain region with a heavy burden of pathology, to determine the impact of GFAP mutation at presymptomatic (3 weeks of age) and severe stages ( 8 weeks of age) of disease. Transcription profiling shows progressive neuroinflammation and neurodegeneration.

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Genetic modifiers of GFAP expression in mouse models of Alexander disease

Project description:Genetic modifiers of GFAP expression in mouse models of Alexander disease

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Microglia sense astrocyte dysfunction and prevent disease progression in an Alexander disease model

Project description:Microglia sense astrocyte dysfunction and prevent disease progression in an Alexander disease model

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Composition of Rosenthal fibers in Alexander disease patients and mouse models

Project description:Alexander disease (AxD) is a fatal neurodegenerative disorder characterized by the presence in astrocytes of protein aggregates called Rosenthal fibers (RFs). In this work, we used a new biochemical fractionation method to enrich for RFs followed by analysis of this fraction using quantitative iTRAQ mass spectrometry. This work identified 77 proteins not previously associated with RFs. Multiple proteins selected for follow-up were confirmed by immunobloting to be enriched in the RF fraction of both the AxD mouse models and human AxD patients including receptor for activated protein C kinase 1 (RACK1), G1/S-specific cyclin D2, and ATP-dependent RNA helicase DDX3X.

2016-05-23 | PXD002448 | Pride

Hippocampal gene expression in the GFAP-R237H rat model of Alexander disease at early and late stages of disease

Project description:Hippocampal gene expression in the GFAP-R237H rat model of Alexander disease at early and late stages of disease

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Aberrant neurodevelopment in human iPS cell-derived models of Alexander disease.

Project description:Aberrant neurodevelopment in human iPS cell-derived models of Alexander disease.

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Aberrant neurodevelopment in human iPS cell-derived neural organoid model of Alexander disease

Project description:3D-cultured unguided neural and cortical organoids derived from human iPS cells carrying a GFAP (R239C) mutation - an identified cause of Alexander disease (AxD) - and their isogenic controls were analyzed with scRNA-seq to investigate the effect of the GFAP mutation on brain development, cell type composition, and gene expression. Results of this analysis showed impaired astro- and neurogenesis in both types of organoids (unguided and cortical), including a lack of cells acquiring the astrocyte fate, and an increased abundance of cells differentiating into lineages other than neuroectodermal. The results also suggested dysregulation of extracellular matrix, membrane, and cytoskeleton components, which might have also affected their differentiation trajectories.

2024-04-07 | GSE261157 | GEO

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