Traumatic insult to the brain leads to a degradation of low molecular weight of cannabinoid type 1 receptor (CB1) and generation of high molecular weight complexes in the cortex and hippocampus, as assessed by both N-terminal and C-terminal specific antibodies. The formation and release of CB1 oligomers was dramatically increased into CSF within 1 hour following traumatic brain insult. Novel CB1 receptor-based, prognostic markers of traumatic brain injury and other forms of brain injury are disclosed. A method of repopulating damaged neural cells by proliferation of a subgroup of neural progenitor cells is described. Targeting CB1 receptors for therapeutic neuroprotection in TBI is also disclosed.