Aetiopathogenesis

Abstract

A growing body of evidence has been collected in recent years regarding the pathogenesis of MSA. The core feature of MSA pathology is the widespread appearance of GCIs containing α-synuclein (αSyn) that correlates significantly with the neuronal deterioration and disease duration. GCIs involve all types of oligodendrocytes (perivascular, perifascicular and perineuronal), illustrating that there is no selective vulnerability of a specific oligodendrocytes. Therefore, MSA is considered an α-synucleinopathy. In addition to the ectopic appearance of αSyn in oligodendrocytes, oxidative stress, mitochondrial dysfunction, excitotoxicity, inflammation, protein conformation and metabolic changes may be important factors contributing to the pathogenesis of MSA.