Parkinson’s disease (PD) is a common neurodegenerative disorder. Moreover, chronic inflammation is found at different stages of PD. Previous studies indicated that environmental inflammatory factors could induce immune responses, release cytokines, especially interleukin-1β(IL-1β), and accelerate the alpha-synuclein (αSyn) pathology. However, the interrelationship between IL-1β, its receptor (IL-1R1) and PD pathogenesis is not understood. This review provides a thorough overview of the links between the IL-1β/ IL-1R1 in neuroinflammation and PD pathogenesis. It summarizes the evidence supporting that inflammation in the CNS or periphery accelerates PD. Finally, the critical molecular mechanisms, particularly IL-1β/ IL-1R1 in PD, are highlighted and discussed. IL-1β in the CNS directly affects the αSyn expression in neurons expressing IL-1R1 to cause the αSyn pathology. Peripheral IL-1βmay accelerate PD progression by recruiting peripheral immune cells, stimulating cells of the blood-brain barrier, and activating IL-1R1 in the brain.

Immunological responses to α-synuclein accumulation in Parkinson’s Disease: an up-to-date review of the literature

Haichen Niu, Email: Niuhc@ice-biosci.com