Traumatic brain injury (TBI) has been associated with an increased risk for neurodegenerative diseases, and Tau spread and accumulation might be one of the mechanisms underlying this process. Exosomes were speculated to be a vehicle for spreading Tau in neurodegenerative diseases. The present study sought to investigate the effect of exosome associated Tau after TBI. C57BL/6J mice were subjected to controlled cortical impact injury and the levels of total and phosphorylated Tau in exosomes were measured. Then we isolated exosomes from wildtype and Tau-knockout mice after TBI. These exosomes were either added to primary cultured neurons to evaluate the toxicity, or injected into brains of mice subjected to TBI to evaluate the effect on brain functions. The levels of total and phosphorylated Tau in exosomes after TBI were significantly elevated. TBI derived exosomes displayed toxicity in primary neuron cultures, exacerbated TBI induced LTP (long-term potentiation) impairment and exacerbated motor and cognitive impairments after TBI. The exosome-associated Tau pathology was one of the mechanisms underlying the long-term neurodegenerative effect after TBI.