In addition, Yoshida et al. [71] recently showed that hippocampal accumulation patterns of p-tau, amyloid-β and pSer129-αSyn may be mutually influenced by coexisting pathologies and although the hippocampi of AD donors in the current study lacked α-synuclein pathology, previous research has shown that α-synuclein co-pathology can drive tau accumulation in AD and potentially accelerate the disease phenotype [91]. The gene discussed is SNCA; the disease is Alzheimer disease.