摘要：

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. •Cerebrovascular dysfunction (CVD) is emerging as a key element in the development of neurodegeneration after TBI.•We propose that TBI initiates CVD, accelerating Aβ/tau deposition and leading to neurodegeneration and dementias.•Clarifying this connection will support the development of novel biomarkers and therapeutic approaches for both TBI and AD. Cerebrovascular dysfunction (CVD) is emerging as a key element in the development of neurodegeneration after TBI. We propose that TBI initiates CVD, accelerating Aβ/tau deposition and leading to neurodegeneration and dementias. Clarifying this connection will support the development of novel biomarkers and therapeutic approaches for both TBI and AD.

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