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Role of Oxidative Stress, Mitochondria Failure, & Cellular Hypoperfusion in the Context of Alzheimer Disease: Past, Present & Fu

Role of Oxidative Stress, Mitochondria Failure, & Cellular Hypoperfusion in the Context of Alzheimer Disease: Past, Present & Fu

9781619428782
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Description
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 Alzheimers 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.
Product Details
Nova Science Publishers Inc
73727
9781619428782
9781619428782

Data sheet

Publication date
2013
Issue number
1
Cover
hard cover
Pages count
426
Dimensions (mm)
260.00 x 180.00
Weight (g)
964
  • 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.
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