Publication Type | Review |
Authors | Ramos-Cejudo J, Wisniewski T, Marmar C, Zetterberg H, Blennow K, de Leon M, Fossati S |
Journal | EBioMedicine |
Volume | 28 |
Pagination | 21-30 |
Date Published | 01/31/2018 |
ISSN | 2352-3964 |
Keywords | Alzheimer Disease, Brain Injuries, Traumatic, Cerebrovascular Circulation |
Abstract | Traumatic brain injury (TBI) and Alzheimer's disease (AD) are devastating neurological disorders, whose complex relationship is not completely understood. Cerebrovascular pathology, a key element in both conditions, could represent a mechanistic link between Aβ/tau deposition after TBI and the development of post concussive syndrome, dementia and chronic traumatic encephalopathy (CTE). In addition to debilitating acute effects, TBI-induced neurovascular injuries accelerate amyloid β (Aβ) production and perivascular accumulation, arterial stiffness, tau hyperphosphorylation and tau/Aβ-induced blood brain barrier damage, giving rise to a deleterious feed-forward loop. We postulate that TBI can initiate cerebrovascular pathology, which is causally involved in the development of multiple forms of neurodegeneration including AD-like dementias. In this review, we will explore how novel biomarkers, animal and human studies with a focus on cerebrovascular dysfunction are contributing to the understanding of the consequences of TBI on the development of AD-like pathology. |
DOI | 10.1016/j.ebiom.2018.01.021 |
PubMed ID | 29396300 |
PubMed Central ID | PMC5835563 |