Yasumasa Yoshiyama

TL;DR: In this paper, the authors studied wild-type and P301S mutant human tau transgenic (Tg) mice and found that tangle formation was preceded by microglial activation.

TL;DR: Data indicate that the R406W mutation causes reduced binding of this mutant tau to microtubules, resulting in slower axonal transport, which leads to increased accumulation and reduced solubility of RW tau in an age-dependent manner, culminating in the formation of filamentous intraneuronal tau aggregates similar to that observed in tauopathy patients.

TL;DR: In conclusion, overexpression of the smallest human brain tau isoform resulted in late onset and age-dependent formation of congophilic tau inclusions with properties similar to those in the tangles of human tauopathies, thereby implicating aging in the pathogenesis of fibrous tAU inclusions.

TL;DR: Compared binding of tau positron emission tomography ligands, PBB3 and AV-1451, by fluorescence, autoradiography and homogenate binding assays with homologous and heterologous blockades using tauopathy brain samples indicate distinct selectivity of P BB3 compared to AV- 1451 for diverse tau fibril strains.

TL;DR: Researchers report studies of the effects of mrTBI on AD-like tau pathologies in Tg mice expressing the shortest human tau isoform (T44) subjected to mmTBI, causing brain concussion without structural brain damage to simulate injuries linked to DP.