Mild traumatic brain injury (mTBI) is the most common type of traumatic brain injury globally. Although its consequences may be short term, mTBI often leads to long-term neuropsychiatric and neurological impairments and has been estimated to increase the probability of later life dementia up to six-fold. It is presently not clear what neuropathological changes underlie these deficits. This talk will review our recent studies on the sustained neurogliovascular unit function changes in a murine model of repeated, mild traumatic brain injury. By leveraging two photon fluorescence microscopy, intracerebral electrophysiological recordings, optogenetics, high field magnetic resonance imaging, and light sheet fluorescence microscopy, we reveal pronounced, lasting, and diffuse changes in the neuronal and cerebrovascular functional signals in situ, accompanied by only subtle changes in histopathological readouts and no changes on conventional neuroimaging. Our studies suggest the potential of disinhibitory interventions to ameliorate peri-contusional neuronal and cerebrovascular tone and reactivity. In light of known import of functional hyperemia for healthy brain functioning, normalization of the neurovascular unit function is likely key for decreasing the susceptibility of the concussed brain to subsequent pathologies. We expect sensitive in situ functional assays to be instrumental for development of such neurovascularly targeted interventions in the clinic.
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