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.
journal_name
EBioMedicinejournal_title
EBioMedicineauthors
Ramos-Cejudo J,Wisniewski T,Marmar C,Zetterberg H,Blennow K,de Leon MJ,Fossati Sdoi
10.1016/j.ebiom.2018.01.021subject
Has Abstractpub_date
2018-02-01 00:00:00pages
21-30issn
2352-3964pii
S2352-3964(18)30025-2journal_volume
28pub_type
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