ArticlebioRxiv : the preprint server for biology2026
Astrocytic ACSBG1 depletion improves lipid-cytokine signaling and attenuates α-Synuclein pathology in a Parkinson's disease mouse model.
Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Astrocytes are key regulators of lipid metabolism, and dysregulated astrocytic lipid processing is implicated in Parkinson's disease (PD) pathogenesis. Our prior genome-wide screens identified ACSBG1, an astrocyte-enriched acyl-CoA synthetase, as a candidate regulator of α-synuclein (α-Syn) levels. However, how ACSBG1 links lipid reprogramming to inflammatory astrocyte activation and α-Syn pathology remains unknown. We compared the transcriptomic, cytokine, and lipid secretomes of TNF-α and IL-1α stimulated primary astrocytes from wild-type (WT) and
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