Pathophysiology of Vascular Cognitive Impairment (I): Theoretical Background
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Vascular cognitive impairment (VCI) describes a spectrum of cognitive changes occurring secondary to damage of the large and small vessels that supply blood to the brain. VCI has been recognized as the second most common cause of dementia and as the most common pathological comorbidity of Alzheimer’s disease. The pathogenesis of VCI appears to be heterogeneous, involving neurodegenerative mechanisms that remain to be fully understood. Stroke and vascular risk factors interfere with many processes subserved by the cerebral vasculature, maintaining cerebral homeostasis (for instance, maintaining and augmenting blood flow, oxygen, glucose supply), providing a structural and chemical barrier between the peripheral circulation and the brain parenchyma, serving intricate immunological functions, and providing a neurogenic niche for brain tissue repair. This chapter discusses the known and theoretical pathophysiological background of VCI, focusing on stroke and disruption of the neurovascular unit (NVU), which contribute to defects in neurotransmitter systems and to disruption of large-scale functionally co-activating networks, which contributes to cognitive deficits and decline.
We would like to gratefully acknowledge the support from our colleagues, Sabrina Adamo and Fuqiang Gao from Sunnybrook Research Institute, for their contribution to the processing and labeling of the MR images. W.S. gratefully acknowledges support from the Alzheimer’s Association (US), Brain Canada, The Canadian Partnership for Stroke Recovery, Sunnybrook Health Sciences Centre Department of Psychiatry, Sunnybrook Research Institute Hurvitz Brain Sciences Program, and the University of Toronto Department of Pharmacology and Toxicology. S.E.B. gratefully acknowledges financial and salary support from the Fondation Leducq, Canadian Institutes of Health Research (#125740 & #13129), Heart and Stroke Foundation Canadian Partnership for Stroke Recovery, Hurvitz Brain Sciences Research Program at Sunnybrook Research Institute, and the Linda C. Campbell Foundation. S.E.B. would also like to thank the Sunnybrook Research Institute, Sunnybrook Health Sciences Centre Department of Medicine, and the Brill Chair Neurology, University of Toronto, for financial and salary support.
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