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. 2025 Mar 18;45(1):26.
doi: 10.1007/s10571-025-01541-5.

A Closer Look at Dystonia with the Glycosylation

Hours Camille  1 , Gressens Pierre  2
Affiliations

A Closer Look at Dystonia with the Glycosylation

Hours Camille et al. Cell Mol Neurobiol. .

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.

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Conflict of interest statement

Declarations. Conflict of interest: The authors have not disclosed any competing interests.

Figures

None
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.
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