Role of α-synuclein in inducing innate and adaptive immunity in Parkinson disease.

Academic Article


  • Alpha-synuclein (α-syn) is central to the pathogenesis of Parkinson disease (PD). Gene duplications, triplications and point mutations in SNCA1, the gene encoding α-syn, cause autosomal dominant forms of PD. Aggregated and post-translationally modified forms of α-syn are present in Lewy bodies and Lewy neurites in both sporadic and familial PD, and recent work has emphasized the prion-like ability of aggregated α-syn to produce spreading pathology. Accumulation of abnormal forms of α-syn is a trigger for PD, but recent evidence suggests that much of the downstream neurodegeneration may result from inflammatory responses. Components of both the innate and adaptive immune systems are activated in PD, and influencing interactions between innate and adaptive immune components has been shown to modify the pathological process in animal models of PD. Understanding the relationship between α-syn and subsequent inflammation may reveal novel targets for neuroprotective interventions. In this review, we examine the role of α-syn and modified forms of this protein in the initiation of innate and adaptive immune responses.
  • Published In


  • Parkinson disease, T-lymphocyte, adaptive immunity, alpha-synuclein, antigen presentation, innate immunity, microglia, post-translational modifications, Adaptive Immunity, Humans, Immunity, Innate, Parkinson Disease, alpha-Synuclein
  • Digital Object Identifier (doi)

    Author List

  • Allen Reish HE; Standaert DG
  • Start Page

  • 1
  • End Page

  • 19
  • Volume

  • 5
  • Issue

  • 1