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Progressive multiple sclerosis

ABSTRACT: Progressive multiple sclerosis

PROVIDER: PRJNA966951 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24422100.fastq.gz	Fastqsanger.gz
	SRR24422101.fastq.gz	Fastqsanger.gz
	SRR24422036_1.fastq.gz	Fastqsanger.gz
	SRR24422036_2.fastq.gz	Fastqsanger.gz
	SRR24422037_1.fastq.gz	Fastqsanger.gz

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Identification of early neurodegenerative pathways in progressive multiple sclerosis

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Identification of early neurodegenerative pathways in progressive multiple sclerosis

Project description:Progressive multiple sclerosis (MS) is characterized by unrelenting neurodegeneration, which causes cumulative disability and is refractory to current treatments. Drug development to prevent disease progression is an urgent clinical need yet is constrained by an incomplete understanding of its complex pathogenesis. Using spatial transcriptomics and proteomics on fresh-frozen human MS brain tissue, we identified multicellular mechanisms of progressive MS pathogenesis and traced their origin in relation to spatially distributed stages of neurodegeneration. By resolving ligand–receptor interactions in local microenvironments, we discovered defunct trophic and anti-inflammatory intercellular communications within areas of early neuronal decline. Proteins associated with neuronal damage in patient samples showed mechanistic concordance with published in vivo knockdown and central nervous system (CNS) disease models, supporting their causal role and value as potential therapeutic targets in progressive MS. Our findings provide a new framework for drug development strategies, rooted in an understanding of the complex cellular and signaling dynamics in human diseased tissue that facilitate this debilitating disease.

2022-06-05 | PXD026529 | Pride

Identification of early neurodegenerative pathways in progressive multiple sclerosis

Project description:Progressive multiple sclerosis (MS) is characterized by unrelenting neurodegeneration, which causes cumulative disability and is refractory to current treatments. Drug development to prevent disease progression is an urgent clinical need yet is constrained by an incomplete understanding of its complex pathogenesis. Using spatial transcriptomics and proteomics on fresh-frozen human MS brain tissue, we identified multicellular mechanisms of progressive MS pathogenesis and traced their origin in relation to spatially distributed stages of neurodegeneration. By resolving ligand–receptor interactions in local microenvironments we discovered defunct trophic and anti-inflammatory intercellular communications within areas of early neuronal decline. Proteins associated with neuronal damage in patient samples showed mechanistic concordance with published in vivo knockdown and CNS disease models, supporting their causal role and value as potential therapeutic targets for progressive MS. Our findings provide a new framework for drug development strategies, rooted in an understanding of the complex cellular and signaling dynamics in human diseased tissue, that facilitate this debilitating disease.

2022-05-12 | GSE174647 | GEO

CSF SERPINA3 levels are increased in patients with progressive multiple sclerosis

Project description:One of the most challenging aspects in multiple sclerosis (MS) research is to understand the mechanisms leading to neurodegeneration and subsequent tissue repair. Here, we aimed to identify biomarkers associated with the progressive phases of the disease that may have neuroprotective potential. To achieve this, we performed a bioinformatic approach integrating transcriptional and proteomic profiles obtained during the course of experimental autoimmune encephalomyelitis (EAE) combined with gene expression microarray data from neuronal differentiation. Integrative analysis of omics data identified two molecules, serine (or cysteine) peptidase inhibitor, clade A, member 3N (Serpina3n) and S100 calcium binding protein A4 (S100A4), as biomarkers up-regulated in chronic progressive EAE whose expression was also induced during neuronal differentiation. Immunofluorescence studies revealed a primarily neuronal expression of Serpina3n and S100A4 during EAE as reflected by their co-localization with β-III-Tubulin in neurons from cerebellum, hippocampus and spinal cord tissues during EAE. Finally, levels of SERPINA3, the human ortholog of murine Serpina3n also known as α1-antichymotrypsin, and S100A4 were increased in cerebrospinal fluid of MS patients compared with non-inflammatory neurological controls. However, only SERPINA3 showed differences across MS clinical forms and levels were significantly elevated in patients with progressive forms of the disease, particularly in patients with primary progressive MS, compared with relapsing-remitting MS and neurological controls. Altogether, these results point to a role of SERPINA3 as biomarker associated with the progressive forms of MS that may also have neuroregenerative potential

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