Vascular dysfunction in the pathogenesis of Alzheimer's disease - A review of endothelium-mediated mechanisms and ensuing vicious circles

Article ID	Journal	Published Year	Pages	File Type
6021582	Neurobiology of Disease	2015	51 Pages	PDF

Abstract

This study reviews the current literature of in vitro and ex vivo studies on endothelium-mediated mechanisms underlying vascular dysfunction in AD pathogenesis, with the aim of presenting a comprehensive overview of the complex network of causative relationships. Particular emphasis is given to vicious circles which can accelerate the process of neurovascular degeneration.

Keywords

NFT GLUT-1 CBF IP3 IFN-γ ET-1 eNOS HIF-1α UPR RNS MCP-1 PKC iNOS NF-kB AQP ICAM-1 LRP-1 ABC TGF-β Ultrastructural damage Aβ precursor protein BACE-1 P-gp AβPP PECAM-1 RAGE mitoKATP TEER Aβ Trans-endothelial electrical resistance Mitochondrial DNA Inositol 1,4,5-triphosphate P-glycoprotein ROS amyloid-β Apoe apolipoprotein E aquaporin Tight junction Mitochondrial dysfunction Endothelial dysfunction endothelin 1 interferon-γ interleukin Alzheimer's disease transforming growth factor-β tumour necrosis factor-α Positron emission tomography cerebral blood flow Neurofibrillary tangle mtDNA BBB Blood–brain barrier inducible nitric oxide synthase endothelial nitric oxide synthase endoplasmic reticulum hypoxia-inducible factor 1α Vascular endothelial growth factor Vascular Endothelial Growth Factor (VEGF)TNF-α nuclear factor kappa B Cerebrospinal fluid CSF intercellular adhesion molecule-1 platelet endothelial cell adhesion molecule 1 Blood–brain barrier permeability Nitric oxide Cerebral hypoperfusion Unfolded protein response PET monocyte chemoattractant protein-1 low-density lipoprotein receptor-related protein 1 Protein kinase C ATP-sensitive potassium channels ATP binding cassette glucose transporter 1 reactive nitrogen species Reactive oxygen species Receptor for advanced glycation end-products