New insights of oligodendrocytes in the etiology of Parkinson’s disease

Abstract

Oligodendrocytes (OLs) are myelin-forming cells in the central nervous system (CNS), providing nutritional and metabolic support to axons. They also interact with other glial cells to regulate the microenvironment of the CNS. Recent clinical studies have revealed that OL dysfunction and white matter changes occur at an early stage of Parkinson’s disease (PD) and may be associated with dopaminergic neuronal damage, postural, and gait disorders. However, whether these changes are primary drivers or secondary consequences of neurodegeneration remains to be determined. Biochemical and genetic studies have provided evidence for OL dysfunction in PD pathology. Mechanistic studies have shown that OL damage can disrupt neuronal integrity through communicating with neurons, and the aggregation of α-synuclein (α-Syn) in OLs also accelerates dopaminergic neuronal death. Emerging evidence suggests that OLs may play a significant role in the pathogenesis and progression of PD through their involvement in mitochondrial damage, oxidative stress, and neuroinflammation. In this review, we summarized current understanding of oligodendrocyte precursor cells (OPCs), OLs, myelination, and white matter in the pathogenesis of PD and discussed the potential therapy by targeting OLs for PD.