title: Oxidative Stress Induced Mitochondrial Failure and Vascular Hypoperfusion as a Key Initiator for the Development of Alzheimer Disease.
abstract: Mitochondrial dysfunction may be a principal underlying event in aging, including age-associated brain degeneration. Mitochondria provide energy for basic metabolic processes. Their decay with age impairs cellular metabolism and leads to a decline of cellular function. Alzheimer disease (AD) and cerebrovascular accidents (CVAs) are two leading causes of age-related dementia. Increasing evidence strongly supports the theory that oxidative stress, largely due to reactive oxygen species (ROS), induces mitochondrial damage, which arises from chronic hypoperfusion and is primarily responsible for the pathogenesis that underlies both disease processes. Mitochondrial membrane potential, respiratory control ratios and cellular oxygen consumption decline with age and correlate with increased oxidant production. The sustained hypoperfusion and oxidative stress in brain tissues can stimulate the expression of nitric oxide synthases (NOSs) and brain endothelium probably increase the accumulation of oxidative stress products, which therefore contributes to blood brain barrier (BBB) breakdown and brain parenchymal cell damage. Determining the mechanisms behind these imbalances may provide crucial information in the development of new, more effective therapies for stroke and AD patients in the near future.
authors.affiliation: School of Health Science and Healthcare Administration, University of Atlanta, 6685 Peachtree Industrial Blvd., Atlanta, Georgia, 30360, USA. galiev@uofa.edu.|Department of Nutrition and Biochemistry, Faculty of Sciences, Javeriana University, Bogotà D.C., Colombia. galiev@uofa.edu.|Stress Relief and Memory Training Center, Brooklyn, New York, NY 11235, USA. galiev@uofa.edu.
authors.forename: Gjumrakch
authors.initials: G
authors.lastname: Aliev
authors.affiliation: Department of Biology, College of Sciences, University of Texas at San Antonio, One UTSA Circle, San Antonio, TX 78249-1664, USA.
authors.forename: Hector H
authors.initials: HH
authors.lastname: Palacios
authors.affiliation: Department of Cytology, Histology and Embryology, Azerbaijan Medical University, 25 Street Bakhikhanov, Baku AZ10 25, Azerbaijan.
authors.forename: Eldar
authors.initials: E
authors.lastname: Gasimov
authors.affiliation: Department of Pathology, School of Medicine, Case Western Reserve University, WRB 5301, Cleveland, Ohio, 44106, USA.
authors.forename: Mark E
authors.initials: ME
authors.lastname: Obrenovich
authors.affiliation: Department of Nutrition and Biochemistry, Faculty of Sciences, Javeriana University, Bogotà D.C., Colombia.
authors.forename: Ludis
authors.initials: L
authors.lastname: Morales
authors.affiliation: Department of Psychiatry, Wroclaw Medical University, 25 St. Kraszewskiego, Wroclaw, 50-229, Poland.
authors.forename: Jerzy
authors.initials: J
authors.lastname: Leszek
authors.affiliation: Stress Relief and Memory Training Center, Brooklyn, New York, NY 11235, USA.
authors.forename: Valentin
authors.initials: V
authors.lastname: Bragin
authors.affiliation: Dirección de Investigación y desarrollo, Centro de Estudios de la Fotosíntesis Humana, S.C. López Velarde 108 y 109, Centro, Aguascalientes, Aguascalientes, 20000, México.
authors.forename: Arturo
authors.initials: A
authors.lastname: Solís Herrera
authors.affiliation: Department of Mathematics, College of Sciences, University of Texas at San Antonio, One UTSA Circle, San Antonio, TX 78249, USA.
authors.forename: Dmitry
authors.initials: D
authors.lastname: Gokhman
keywords: Alzheimer disease; antioxidants; hypometabolism; metabolism; mitochondria; neurodegeneration; oxidative stress