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Role of Oxidative Stress, Mitochondria Failure, & Cellular Hypoperfusion in the Context of Alzheimer Disease

Autor Gjumrakch Aliev
en Limba Engleză Hardback – mai 2013
Atherosclerosis and stroke are two leading causes of age-associated disability, dementia, and death. The Centers for Disease Control and Prevention (CDC) and the National Center for Health Statistics recently reported that Alzheimer's Disease has surpassed diabetes as a leading cause of death. Alzheimer is now the sixth-leading cause of death in the United States. This book discusses the roles of oxidative stress, mitochondria failure, and cellular hypoperfusion in the context of Alzheimer Disease.
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Specificații

ISBN-13: 9781619428782
ISBN-10: 1619428784
Pagini: 426
Ilustrații: Illustrations
Dimensiuni: 184 x 260 x 28 mm
Greutate: 0.96 kg
Ediția:New.
Editura: Nova Science Publishers Inc

Cuprins

Preface; Are Mitochondrial Failures a Key Component in Alzheimer Disease?; In Vivo & in Vitro Assessment of the Brain Mitochondrial Bioenergetics in Aging Rats; The Pathophysiology of Cerebrovascular Lesions in Alzheimer Disease; Vascular Pathology in the Pathogenesis of Alzheimer Disease; Oxidative Stress Induced Mitochondrial Failure & Cellular Hypoperfusion as Primary Pathogenic Factors for the Development & Progression of Alzheimer Disease; The Relationship between the Oxidative Stress Induced Mitochondrial Failure & Vascular Hypoperfusion as a Key Initiator for the Development of Alzheimer Disease; The Relationship between Ischemic Stroke, Oxidative Stress Induced Mitochondrial Failure, & Brain Hypoperfusion in the Context of Vascular Disorder with Neurodegenerative Consequences; Atherosclerotic Lesions & Mitochondria DNA Deletions as a Primary Hallmark of the Brain Microcirculation: Implication in the Pathogenesis of Alzheimer Disease; The Three-Vessel Occlusion as a Model of Vascular Dementia: Oxidative Stress & Mitochondrial Failure as an Initiator of Brain Hypoperfusion; Nitric Oxide as an Accelerator & Initiator of Brain Lesions During the Development of Alzheimer Disease; The Effect of Chronic Brain Hypoperfusion on the of Vascular Nitric Oxide Activities Associates with the Spatial memory & NOS Enzymes Activities; The Selective Loss of GRK2 Regulation & Consequent Cerebrovascular Complications & Alzheimer Disease; The Role of Antioxidants in Health & Age-Associated Diseases; Oxidative Stress Induced Mitochondrial DNA Deletion as a Primary Hallmark for the Drug Development in the Context of Cerebrovascular Diseases; Preventive & Therapeutic Effects of the Coenzyme Q10 Supplementation in a Rat Model of Cerebral Ischemia-Reperfusion; Potential Preventive Effects of Coenzyme Q & Creatine Supplementation on Brain Energy Metabolism in Rats Exposed to Chronic Cerebral Hypoperfusion; Acetyl-L-Carnitine & Lipoic Acid as Treatment Options for the Amelioration of the Neuronal Mitochondria in Aged Rats; The Protective Effect of R-¨»-Lipoic Acid & Acetyl-L-Carnitine Regiments in ApoE4 Mice as Models for Alzheimer Disease; Implication of the Flavones from the Root of Scutellaria Baicalensis Georgi as New & More Effective Drugs for the Treatment of Neurodegeneration; Implication of Oncogenic Signaling Pathways as a Treatment Strategy for Neurodegeneration; The Integrated Treatment Approach of the Cognitive Function in Demented & Clinically Depressed Patients; Index.