Several studies reported that tau alone was sufficient to provoke severe neurodegeneration leading to parkinsonism in the absence of synucleinopathy in frontotemporal dementia and postencephalitic parkinsonism subjects.43–45 Together, these data support a mechanism where phosphorylated-tau accumulations may be an important, and indeed early, pathogenic contributor to PD, although the requirement for tau leading to a nigral synucleinopathy will need to be established.31 This evidence concerns the gene MAPT and frontotemporal dementia.