This finding might mirror the continuum of Lewy body pathology observed in patients with PD and DLB,14 with the most pronounced Lewy body pathology in DLB patients, especially when exhibiting variants in GBA1. 11A proinflammatory condition preceding and/or induced by Lewy bodies might lead to the local deposition of TF, similar to the situation observed in senile plaques in AD, causing reduced levels of TF in the CSF of patients, analogous to the reduced CSF levels of α-Synuclein found in PD patients. The gene discussed is TF; the disease is Alzheimer disease.