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

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    0571245 - ÚEM 2024 RIV US eng J - Journal Article
    Filipi, Tereza - Matúšová, Zuzana - Abaffy, Pavel - Vaňátko, Ondřej - Turečková, Jana - Benešová, Šárka - Kubísková, Monika - Kirdajová, Denisa - Zahumenský, Jakub - Valihrach, Lukáš - Anděrová, Miroslava
    Cortical glia in SOD1(G93A) mice are subtly affected by ALS-like pathology.
    Scientific Reports. Roč. 13, april (2023), č. článku 6538. ISSN 2045-2322. E-ISSN 2045-2322
    R&D Projects: GA ČR(CZ) GA23-05327S; GA ČR(CZ) GA19-02046S; GA MŠMT(CZ) ED1.1.00/02.0109; GA MŠMT(CZ) LX22NPO5107; GA MŠMT(CZ) LM2023050
    Institutional support: RVO:68378041 ; RVO:86652036
    Keywords : amyotrophic-lateral-sclerosis * motor-neuron degeneration * transgenic mouse model * differential expressiongene-expression * spinal-cord * microglia * disease * astrocytes * activation
    OECD category: Neurosciences (including psychophysiology
    Impact factor: 4.6, year: 2022
    Method of publishing: Open access
    https://www.nature.com/articles/s41598-023-33608-y

    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 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 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 support the hypothesis that the SOD1(G93A) mouse 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.
    Permanent Link: https://hdl.handle.net/11104/0342519

     
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