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Effects of neuron-derived a-synuclein in oligodendrocytes [RNA-Seq]

GSE312641 Mus musculus Expression profiling by high throughput sequencing 9 samples Submitted 2025/12/10 Platform GPL16790
Summary
Synucleinopathies, including multiple system atrophy (MSA) and Parkinson's disease (PD), are characterized by intracellular accumulation of α-synuclein (αSyn) aggregates. Despite oligodendrocytes' low expression of αSyn, αSyn aggregates in MSA cause glial cytoplasmic inclusions (GCIs). Here, we show that GCI development is facilitated by αSyn propagation from neurons to oligodendrocytes via Toll-like receptor 2 (TLR2). Demyelination-related characteristics in MSA oligodendrocytes and experimental models were identified by transcriptome studies. NM-101 treatment reversed the demyelination phenotype in the transgenic mouse model. These results point to anti-TLR2 immunotherapy as a possible MSA disease-modifying strategy.
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Direct links to NCBI, no account and no request form: the whole study as GSE312641_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 9 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1180266 and SRA study SRP542299. Searching any of these in the dataset finder brings you back here.

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