Emerging evidence suggests that prion-like α-synuclein (α-syn) cell-to-cell transmission is an important driver in the pathogenesis of Parkinson's disease (PD). Recently, we discovered LAG3 as the receptor of pathological α-syn transmission (1). Furthermore, internalized pathological α-syn caused PARP-1 activation and PAR accumulation, which converted α-syn into a more toxic strain and accelerated neurotoxicity (2). Depletion/inhibition of LAG3 or PARP-1 can substantially inhibit α-syn-induced neurodegeneration.<br/><br/>

Transmission mechanism of pathological alpha-synuclein

2019 Fall National Meeting

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