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. The gene discussed is TARDBP; the disease is Urinary incontinence.