Tauopathy has been linked to the pathogenesis of neurodegenerative diseases including Alzheimer's disease (AD) and Parkinson disease (PD). Our previous research indicates that interactions between dopamine and oxidative damage in the striatum are involved in the late-stages of neurodegenerative diseases, and distinct density change patterns in translocator protein (TSPO) may associate with microglia dystrophy in neurodegeneration. We investigated whether microglia dystrophy is associated with oxidative damage thus effecting the pathological spread of tau and finally tau proteostasis disturbances. This study investigated TSPO and Tau densities in the caudate and putamen of 65 postmortem human brains using autoradiography in PD, PDD, DLB, AD, and controls. Sample concentrations of myeloperoxidase (MPO), poly (ADP-Ribose) (PAR), and triggering receptors expressed on myeloid cell 2 (TREM2) were determined via ELISA. All samples were genotyped for TSPO, TREM2, and bridging integrator 1 (BIN1) using SNP Assays. TREM2 gene variants were absent. The associations between TSPO and BIN1 gene polymorphisms and TSPO, MPO, TREM2, and PAR level variations were found - potentially elucidating the interrelationship of relevant biological events. Significantly lower PAR levels were found in all LBD caudate samples (PD, PDD, and DLB). TSPO and Tau densities in LBD brains were remarkably lower, these levels increased in AD cases. These data provide evidence that microglia dystrophy in LBD cases, in contrast to AD, are mainly a result of oxidative damage induced by misfolded tau proteins causing reduced tau propagation and proteostasis disturbances. Results indicate BIN1 gene G allele SNPs as a potential risk factor for tauopathy.