Affiliations: [a] Department of Biochemistry, Medical, Pharmaceutical & Toxicological Chemistry, Krasnoyarsk State Medical University, Krasnoyarsk, Russia | [b] Department of Ambulatory Therapy and Family Medicine, Krasnoyarsk State Medical University, Krasnoyarsk, Russia
Correspondence:
[*]
Correspondence to: Alla B. Salmina, Department of Biochemistry, Medical, Pharmaceutical and Toxicological Chemistry, Krasnoyarsk State Medical University named after Prof. V.F.Voino-Yasenetsky, P.Zheleznyaka str., 1, Krasnoyarsk, 660022, Russia. Tel.: +7 391 2280769; Fax: +7 391 2201071; E-mail: [email protected].
Note: [] Handling Associate Editor: Alexander Boldyrev
Abstract: Current theories state that Alzheimer's disease (AD) is a vascular disorder that initiates its pathology through cerebral microvascular abnormalities. Endothelial dysfunction caused by the injury or death of endothelial cells contributes to progression of AD. Also, functional relationships between neurons, glial cells, and vascular cells within so-called neurovascular unit are dramatically compromised in AD. Several recent studies have highlighted that endothelial cells might be the target for the toxic action of heavily aggregated proteins, glia-derived cytokines, and stimuli inducing oxidative and metabolic stress in AD brains. Here, we describe the properties of the brain endothelium that contribute to its specific functions in the central nervous system, and how endothelial-neuronal-glial cell interactions are compromised in the pathogenesis of AD. We also discuss the ways in which functioning of endothelial cells can be modulated in cerebral microvessels. Understanding of molecular mechanisms of endothelial injury and repair in AD would give us novel diagnostic biomarkers and pharmacological targets.
