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Review
. 2017 Mar:34:77-87.
doi: 10.1016/j.arr.2016.09.006. Epub 2016 Sep 30.

Dysfunction of the neurovascular unit in ischemic stroke and neurodegenerative diseases: An aging effect

Wei Cai  1 , Kai Zhang  2 , Peiying Li  3 , Ling Zhu  4 , Jing Xu  2 , Boyu Yang  2 , Xiaoming Hu  2 , Zhengqi Lu  5 , Jun Chen  6
Affiliations
Review

Dysfunction of the neurovascular unit in ischemic stroke and neurodegenerative diseases: An aging effect

Wei Cai et al. Ageing Res Rev. 2017 Mar.

Abstract

Current understanding on the mechanisms of brain injury and neurodegeneration highlights an appreciation of multicellular interactions within the neurovascular unit (NVU), which include the evolution of blood-brain barrier (BBB) damage, neuronal cell death or degeneration, glial reaction, and immune cell infiltration. Aging is an important factor that influences the integrity of the NVU. The age-related physiological or pathological changes in the cellular components of the NVU have been shown to increase the vulnerability of the NVU to ischemia/reperfusion injury or neurodegeneration, and to result in deteriorated brain damage. This review describes the impacts of aging on each NVU component and discusses the mechanisms by which aging increases NVU sensitivity to stroke and neurodegenerative diseases. Prophylactic or therapeutic perspectives that may delay or diminish aging and thus prevent the incidence of these neurological disorders will also be reviewed.

Keywords: Aging; Ischemic stroke; Neurodegeneration; Neurovascular unit; Vulnerability.

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Figures

Figure 1
Figure 1
Schematic of neurovascular unit components.
Figure 2
Figure 2
Brief summary of interactions among neurovascular unit components.
Figure 3
Figure 3
General pathophysiological phases of ischemic stroke. There are three pathophysiological phases after the onset of ischemic stroke: the excitotoxicity phase, the inflammatory phase, and the chronic phase.
Figure 4
Figure 4
Two-hit hypothesis of Alzheimer’s disease. The two-hit hypothesis of Alzheimer’s disease proposed a view that vascular risk factors and cell cycle-related abnormalities could lead to AD synergistically. As the first hit, the aged-related vascular risk factors impair the NVU function and result in hypoperfusion and hypoxia infraction. The second hit comes from the abnormal accumulation of amyloid-β (Aβ), which is caused by increased production and reduced clearance of Aβ. The NVU damage and Aβ accumulation together accelerate neurodegeneration and dementia in Alzheimer’s disease.
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