We have provided direct evidence that rmTBI in mice is sufficient to induce a wide range of neuropathological features resembling those in human CTE, including axonal pathology, tau, APP, and TDP-43 pathologies, neuroinflammation, neuronal loss, white matter degeneration and cerebellar pathology, as well as clinically relevant functional deficits, including sensorimotor coordination imbalance, urinary incontinence, and cognitive deficit. This evidence concerns the gene MAPT and Cognitive impairment.