MAPT and Stroke: The resultant hyperphosphorylation of tau enhances its resistance to degradation, maintains the pathogenic cis stereo-isoform of P-tau231 (cis P-tau), inhibits its physiologic function, and propagates the neuropathological cistauosis characteristic of neurodegenerative diseases such as AD, CTE after TBI, vascular contribution to cognitive impairment and dementia (VCID) or vascular dementia (VaD) after stroke long before tangle formation [30,36,43,44,48].