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Host Genetics and Gut Microbiota Influence Lipid Metabolism and Inflammation: Potential implications for ALS Pathophysiology in SOD1 G93A Mice

ABSTRACT: Host Genetics and Gut Microbiota Influence Lipid Metabolism and Inflammation: Potential implications for ALS Pathophysiology in SOD1 G93A Mice

PROVIDER: PRJNA1169339 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30893200_1.fastq.gz	Fastqsanger.gz
	SRR30893200_2.fastq.gz	Fastqsanger.gz
	SRR30893201_1.fastq.gz	Fastqsanger.gz
	SRR30893201_2.fastq.gz	Fastqsanger.gz
	SRR30893202_1.fastq.gz	Fastqsanger.gz

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Expression data from mutant SOD1(G93A) transgenic mice

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Cortical glia in SOD1(G93A) mice are subtly affected by ALS-like pathology

Project description:The role of glia in amyotrophic lateral sclerosis (ALS) is undeniable. Their disease-related activity has been extensively studied in the spinal cord, but only partly in the brain. We present herein a comprehensive study of glia in the motor cortex of SOD1(G93A) mice – a widely used model of ALS. Using single-cell RNA sequencing (scRNA-seq) and immunohistochemistry, we inspected astrocytes, microglia and oligodendrocytes, in four stages of the disease, respecting the factor of sex. We report insignificant motor neuron loss in the cortex, and likewise, minimal changes of glia throughout the disease progression and regardless of sex. Pseudobulk and single-cell analyses revealed subtle disease-related transcriptional alterations at the end-stage in microglia and oligodendrocytes, which were supported by immunohistochemistry. Therefore, our data conclusively prove that the SOD1(G93A) mouse motor cortex does not recapitulate the disease in patients, and we recommend the use of a different model for future studies of the cortical ALS pathology.

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miRNA expression in fast and slow skeletal muscle of wild type and SOD1-G93A mice

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