Current and Future Treatments of Vascular Cognitive Impairment

Abstract

Nonamyloid sporadic cSVD is considered the most prevalent cause or pathological substrate of VCI. 20,21 It refers to diseased microscopic perforating cerebral arterioles, capillaries, and venules giving rise to abnormalities in the cerebral white and deep gray matter. 5 Driven by arteriosclerosis and fibrinoid necrosis, the arteriolar wall can be stenosed, occluded, dilated, or ruptured, which may result in lacunar infarcts or deep microparenchymal/macroparenchymal hemorrhages. 22 In addition, recent studies suggested that cSVD is a dynamic process that affects the whole brain, beginning at the cellular level that involves the components of neurovascular units, including endothelial cells, pericytes, vascular smooth muscle cells, glia, neurons, immune cells, and extracellular matrix. 23,24 These units regulate cerebral blood flow, endothelial function, BBB integrity, and neuroinflammation. 5,23,25 Endothelial dysfunction, astrocytopathy, and BBB leakage may occur when components of neurovascular units are diseased or damaged due to aging, vascular risk factors (eg, hypertension, hyperlipidemia, hyperhomocysteinemia, diabetes, smoking), 26,27 increase in pulsatile flow being transmitted to the cerebral small vessels secondary to aortic stiffness, 28 and genetic factors. 5,24,29,30 These pathological changes may lead to compromised cerebral

Introduction to Focused Update Vascular Cognitive Impairment and Dementia: Better Diagnosis, More Avenues for Prevention

“…There are no Food and Drug Administration-approved treatments specific to VCID. In this issue, Ip et al 15 summarize the status of VCI treatment and provide suggestions for new target discovery.…”