A Closer Look at Dystonia with the Glycosylation
- PMID: 40102359
- PMCID: PMC11920444
- DOI: 10.1007/s10571-025-01541-5
A Closer Look at Dystonia with the Glycosylation
Abstract
Glycosylation, Cellular Stress, and Immunity in Dystonia Pathogenesis. Glycosylation, cellular stress (eIF2α activation), and immune dysfunction converge to disrupt neuronal function and contribute to the pathogenesis of dystonia. Defective glycosylation can lead to oxidative stress, cellular apoptosis, and immune dysfunction, just as oxidative stress, cellular apoptosis, and immune dysfunction can lead to defective glycosylation. These processes, including ER stress and autophagy, interact with glycosylation and immune responses, leading to a better understanding of the molecular mechanisms underlying this neurodevelopmental disorder.
Conflict of interest statement
Declarations. Conflict of interest: The authors have not disclosed any competing interests.
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