Fig. 1.

TBI and AD are connected in a complex interplay.

Experimental data shows that Aβ and tau release leads to cerebrovascular injury and that their deposition around cerebral microvessels has a deleterious chronic effect. Secondarily, cerebrovascular injury is known to induce Aβ and tau deposition in a feedback loop that ultimately may lead to cognitive impairment and the development of AD-like pathology. Together with Aβ and tau accumulation, TBI induces endothelial cell (EC) damage, a modulation on junction proteins (JPs) and matrix metalloproteinase (MMPs) expression and ultimately an impairment of blood brain barrier (BBB) permeability. Because TBI is a relatively homogeneous disease compared to AD, analyzing biomarkers of TBI and their relationship with post-concussive symptoms and dementia offers a promising framework to better understand the relationship between cerebrovascular dysfunction (CVD) and the development of dementia.