Fig. 20

Hypothetical scheme for how early vascular injury leads to a delayed and chronic neurobehavioral phenotype. Blast exposure is associated with an early and selective vascular injury [27] associated with damage to and loss of perivascular astrocytes [29] with altered vascular extracellular matrix proteins ([27, 29, this paper], leading to presumed blood brain barrier dysfunction. Perivascular and neuronal tau accumulation is an early feature of the injury [21]. Late neuroinflammation (initially perivascular) and synaptic loss appear together with neurobehavioral alterations) [31, 33, this paper]. The resulting PTSD-like phenotype has at least in part a glutamatergic basis as it is rescued with a metabotropic glutamate receptor 2/3 antagonist [65]