Traumatic Brain Injury and Alzheimer's Disease: The Cerebrovascular Link

Jaime Ramos-Cejudo, Thomas Wisniewski, Charles Marmar, Henrik Zetterberg, Kaj Blennow, Mony J de Leon, Silvia Fossati, Jaime Ramos-Cejudo, Thomas Wisniewski, Charles Marmar, Henrik Zetterberg, Kaj Blennow, Mony J de Leon, Silvia Fossati

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.

Keywords: Alzheimer's disease; Aβ; Biomarkers; Cerebrovascular pathology; Tau; Traumatic brain injury.

Copyright © 2018 The Authors. Published by Elsevier B.V. All rights reserved.

Figures

Fig. 1
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.
Fig. 2
Fig. 2
Biomarker studies to understand the cerebrovascular link between TBI and AD. Multimodal biomarker studies can be used to better understand the complex interplay between TBI and the development of AD-like pathology. TBI induces early and subacute cerebrovascular function impairment that can be monitored by neuroimaging techniques. This includes blood flow impairment, hypoperfusion and ischemia, changes in brain metabolism and also an impairment of brain clearance systems. If these phenomena are not isolated but sustained because of repeated TBI events or severe TBI, secondary cerebrovascular damage can occur, including vascular damage, BBB abnormal permeability and microbleeds that can be also detected by neuroimaging techniques. Cerebrovascular function impairment and damage induce perivascular and parenchymal accumulation of tau and Aβ in the brain. All these processes act in a feed-forward loop, as an increase in perivascular accumulation of tau and Aβ induce vascular damage, limits vascular function and therefore impairment in blood flow and brain perfusion. These events induce changes in CSF, peripheral blood and biofluids molecules like tau, P-Tau, Aβ monomers/oligomers, metalloproteases and miRNAs, among others.
Fig. 3
Fig. 3
Molecular events involved in cerebrovascular dysfunction. TBI and AD share certain pathological features where cerebrovascular dysfunction (CVD) plays a fundamental role. (Left) Cerebrovascular alterations taking place in the context of the neurovascular unit (NVU) in TBI and AD. (Right) Recent works in TBI and AD showing cerebrovascular alterations. Rev: Reviewed in.

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