In turn, α-synuclein was observed to interact with, and mislocalize, DNMT1 (Desplats et al., 2011) which may contribute to hypomethylation and further activation of SNCA. These interactions constitute a putative positive feedback loop that could contribute to late α-synuclein accumulation, and consequent PD, following an initial increase due to TBI. Here, SNCA is linked to Parkinson disease.