SNCA and Parkinson disease: However, the lack of α-synuclein pathology observed beyond a few months post-injury [69, 196] casts doubt over whether TBI could indeed play a role in initiating and perpetuating chronic α-synuclein accumulation, aggregation and spread, such as that seen in PD, or whether this is simply an acute response to injury that mimics some features of chronic neurodegenerative diseases.