Traumatic brain injury (TBI) induces blood-brain barrier (BBB) disruption, which contributes
to secondary injury of brain tissue and development of chronic cognitive decline.
However, single mild (m)TBI, the most frequent form of brain trauma disrupts the BBB
only transiently. We hypothesized, that co-morbid conditions exacerbate persistent
BBB disruption after mTBI leading to long term cognitive dysfunction. Since hypertension
is the most important cerebrovascular risk factor in populations prone to mild brain
trauma, we induced mTBI in normotensive Wistar and spontaneously hypertensive rats
(SHR) and we assessed BBB permeability, extravasation of blood-borne substances, neuroinflammation
and cognitive function two weeks after trauma. We found that mTBI induced a significant
BBB disruption two weeks after trauma in SHRs but not in normotensive Wistar rats,
which was associated with a significant accumulation of fibrin and increased neuronal
expression of inflammatory cytokines TNFα, IL-1β and IL-6 in the cortex and hippocampus.
SHRs showed impaired learning and memory two weeks after mild TBI, whereas cognitive
function of normotensive Wistar rats remained intact. Future studies should establish
the mechanisms through which hypertension and mild TBI interact to promote persistent
BBB disruption, neuroinflammation and cognitive decline to provide neuroprotection
and improve cognitive function in patients with mTBI.