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LOSS OF DJ-1 AND PARKIN IN PARKINSON’S DISEASE OLIGODENDROCYTES INDUCES OXIDATIVE STRESS AND IMPAIRS DIFFERENTIATION AND MYELINATION
Jose Maria Salazar Camposand 3 co-authors
Biomedical Center (BMC), Faculty of Medicine, LMU Munich
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS03-08AM-064
Presentation
Date TBA
Board: PS03-08AM-064
Event Information
Poster Board
PS03-08AM-064
Poster
View posterAbstract
Parkinson’s disease (PD) has traditionally been viewed as a purely neuronal disorder, primarily characterized by degeneration of dopaminergic neurons in the substantia nigra. Growing evidence now indicates that glial cells, particularly oligodendrocytes (OLs), also contribute critically to PD pathogenesis. Recent studies have identified PD risk factors linked not only to dopaminergic neurons but also to OLs. Yet it remains unclear how OL-specific mechanistic pathways differ between PD and healthy brains, and which OL functions and cellular pathways contribute to midbrain neuron vulnerability.
To explore a potential causal role for OLs in PD aetiology, we generated PD patient-derived and CRISPR-engineered OLs from induced pluripotent stem cells (iPSCs) with loss of the PD-linked genes DJ-1 or parkin. In these cells, we uncovered reduced differentiation into both early and mature OLs, accompanied by oxidative stress and mitochondrial dysfunction, which was reversible upon correction of the DJ-1 mutation. Analysis of PD patient brain tissue confirmed decreased myelination, and transplantation of DJ-1-deficient OLs into ex vivo mouse brain slices likewise resulted in impaired myelination capacity. Collectively, our study shows how PD-associated mutations compromise OL functionality by affecting maturation, cellular stress responses, and myelin formation. These findings highlight a critical contribution of OLs to PD pathology, and suggest that restoring OL function may offer new therapeutic avenues for PD.
To explore a potential causal role for OLs in PD aetiology, we generated PD patient-derived and CRISPR-engineered OLs from induced pluripotent stem cells (iPSCs) with loss of the PD-linked genes DJ-1 or parkin. In these cells, we uncovered reduced differentiation into both early and mature OLs, accompanied by oxidative stress and mitochondrial dysfunction, which was reversible upon correction of the DJ-1 mutation. Analysis of PD patient brain tissue confirmed decreased myelination, and transplantation of DJ-1-deficient OLs into ex vivo mouse brain slices likewise resulted in impaired myelination capacity. Collectively, our study shows how PD-associated mutations compromise OL functionality by affecting maturation, cellular stress responses, and myelin formation. These findings highlight a critical contribution of OLs to PD pathology, and suggest that restoring OL function may offer new therapeutic avenues for PD.
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