Furthermore, aSyn might intracellularly aggregate in Lewy bodies and presynaptic terminals (thereby possibly decreasing the extracellular amount), since results from studies on aSyn in patients with AD have been somewhat heterogeneous, perhaps indicating a subgroup of AD patients with additional Lewy body pathology and a clear mismatch of high p-tau protein 181 and low aSyn CSF levels [71]. The gene discussed is MAPT; the disease is Alzheimer disease.