Prion-Like Propagation of Post-Translationally Modified Tau in Alzheimer’s Disease: A Hypothesis

摘要: The microtubule-associated protein Tau plays a key role in the neuropathology of Alzheimer’s disease by forming intracellular neurofibrillary tangles. normal physiological condition helps stabilize microtubules and transport. aggregates due to various gene mutations, insults abnormal post-translational modifications, phosphorylation being most important one. Other modifications which alter function are glycation, nitration, acetylation, methylation, oxidation, etc. In addition aggregates, pathology might spread prion-like manner as revealed several vitro vivo studies. possible mechanism can be via bulk endocytosis misfolded species. recent studies elucidating this have mainly focussed on aggregation repeat domain cell culture models. Further needed elucidate propagation property full-length its more intense well conditions. Varied discrete effects propensity propagation. Here, we review properties hypothesize glycation Tau. This post-translationally modified an enhanced differential conferred modifications.