Journal
EBIOMEDICINE
Volume 28, Issue -, Pages 21-30Publisher
ELSEVIER
DOI: 10.1016/j.ebiom.2018.01.021
Keywords
Traumatic brain injury; Alzheimer's disease; Cerebrovascular pathology; Biomarkers; A beta; Tau
Funding
- American Heart Association [13SDG16860017]
- Blas Frangione Foundation New Investigator Grant
- Leon Levy Fellowship in Neuroscience
- MDL's grants [NIH AG022374, AG013616, AG012101, AG008051, RF1057570]
- Cohen Veterans Bioscience
- NIH [AG008051, NS073502]
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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 amechanistic link between A beta/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 beta (A beta) production and perivascular accumulation, arterial stiffness, tau hyperphosphorylation and tau/A beta-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 hownovel 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. (c) 2018 The Author(s). Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license
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