Role of oxidative stress, mitochondria failure, and cellular hypoperfusion in the context of Alzheimer disease : past, present and future [E-Book]
Series: Neurology--laboratory and clinical research development series | Aging issues, health and financial alternatives seriesPublisher: New York : Nova Science Publishers, Inc, [2013]Description: 1 online resourceContent type:- text
- computer
- online resource
- 9781619428973
- 1619428970
Contents:
THE ROLE OF OXIDATIVE STRESS, MITOCHONDRIA FAILURE, AND CELLULAR HYPOPERFUSION IN THE CONTEXT OF ALZHEIMER DISEASE ; THE ROLE OF OXIDATIVE STRESS, MITOCHONDRIA FAILURE, AND CELLULAR HYPOPERFUSION IN THE CONTEXT OF ALZHEIMER DISEASE ; Dedication and Acknowledgments ; Contents ; Preface ; Are Mitochondrial Failures a Key Component in Alzheimer Disease? ; Abstract ; Acknowledgments ; References ; In Vivo and In Vitro Assessment of the Brain Mitochondrial Bioenergetics in Aging Rats ; Abstract ; Introduction ; Materials and Methods ; Animals ; Methods.
In vivo 31P Magnetic Resonance Spectroscopy In Vitro Mitochondrial Respiration ; In Vitro Mitochondrial Oxidative Phosphorylation (Table 2 and Figure 2) ; Endogenous Antioxidants ; Statistical Methods ; Results ; In Vivo 31P Magnetic Resonance Spectroscopy ; Endogenous Antioxidants (Table 3 and Figure 3) ; Discussion ; Acknowledgments ; References ; The Pathophysiology of Cerebrovascular Lesions in Alzheimer Disease ; Abstract ; The Effect of Oxidative Stress on Brain Microvessel Function in AD ; Neuropathologic Features of Cerebrovascular Lesions.
Hypoperfusion as a Factor in the Development of AD Relationships between Apolipoprotein E (ApoE) Genotype, Hypercholesterolemia, and Vascular Changes in AD ; Hypoxia/Ischemia/Reperfusion as Cofactors for Oxidative Stress Induced Cerebrovascular Lesions and their Relationship to AD ; The Role of Mitochondrial Abnormalities in the Patho-Genesis of Oxidative Stress-Induced Brain Lesions in AD ; The Role of Endothelial Vasoactive Substancesin the Pathophysiology of Brain Ischemia/Reperfusion and AD ; Transgenic Animals as Models for Studying Cerebrovascular Lesions in AD.
Prevention of AD Using Selective Pharmacological Treatments Conclusion and Considerations for the Future; Acknowledgments ; References ; Vascular Pathology in the Pathogenesis of Alzheimer Disease ; I. Epidemiological Findings ; II. Elements of Brain Tissue Metabolism; III. Causes and Risk Factors ; Inflammatory System ; Vascular Pathology ; 1. Mitochondrial Dysfunction in AD ; 2. Hypoxia and AD ; 3. History of Stroke, Cerebral Ischemia and AD ; 4. Hypertension and Alzheimer Disease ; Acknowledgments ; References.
Oxidative Stress Induced Mitochondrial Failure and Cellular Hypoperfusion as Primary Pathogenic Factors for the Development and Progression of Alzheimer Disease Abstract ; Introduction ; Cerebral Vascular Energy Requirements: Hypoperfusion as a Key Factor for the Development of AD ; The Effect of Oxidative Stress on Brain Microvessel Function and A<U+00dd> Deposition in AD; Morphometric and Neuropathological Features of CerebroVascular Lesions and A<U+00dd> in AD ; Relationships between ApoE Genotype, Hypercholesterolemia, A<U+00dd> and Vascular Changes in AD.
| Item type | Home library | Class number | URL | Status | Date due | Barcode | |
|---|---|---|---|---|---|---|---|
| Electronic book | Stenhouse Library (Kingston Hospital) Online | Link to resource | Available |
Includes bibliographical references and index.
Description based on print version record.
THE ROLE OF OXIDATIVE STRESS, MITOCHONDRIA FAILURE, AND CELLULAR HYPOPERFUSION IN THE CONTEXT OF ALZHEIMER DISEASE ; THE ROLE OF OXIDATIVE STRESS, MITOCHONDRIA FAILURE, AND CELLULAR HYPOPERFUSION IN THE CONTEXT OF ALZHEIMER DISEASE ; Dedication and Acknowledgments ; Contents ; Preface ; Are Mitochondrial Failures a Key Component in Alzheimer Disease? ; Abstract ; Acknowledgments ; References ; In Vivo and In Vitro Assessment of the Brain Mitochondrial Bioenergetics in Aging Rats ; Abstract ; Introduction ; Materials and Methods ; Animals ; Methods.
In vivo 31P Magnetic Resonance Spectroscopy In Vitro Mitochondrial Respiration ; In Vitro Mitochondrial Oxidative Phosphorylation (Table 2 and Figure 2) ; Endogenous Antioxidants ; Statistical Methods ; Results ; In Vivo 31P Magnetic Resonance Spectroscopy ; Endogenous Antioxidants (Table 3 and Figure 3) ; Discussion ; Acknowledgments ; References ; The Pathophysiology of Cerebrovascular Lesions in Alzheimer Disease ; Abstract ; The Effect of Oxidative Stress on Brain Microvessel Function in AD ; Neuropathologic Features of Cerebrovascular Lesions.
Hypoperfusion as a Factor in the Development of AD Relationships between Apolipoprotein E (ApoE) Genotype, Hypercholesterolemia, and Vascular Changes in AD ; Hypoxia/Ischemia/Reperfusion as Cofactors for Oxidative Stress Induced Cerebrovascular Lesions and their Relationship to AD ; The Role of Mitochondrial Abnormalities in the Patho-Genesis of Oxidative Stress-Induced Brain Lesions in AD ; The Role of Endothelial Vasoactive Substancesin the Pathophysiology of Brain Ischemia/Reperfusion and AD ; Transgenic Animals as Models for Studying Cerebrovascular Lesions in AD.
Prevention of AD Using Selective Pharmacological Treatments Conclusion and Considerations for the Future; Acknowledgments ; References ; Vascular Pathology in the Pathogenesis of Alzheimer Disease ; I. Epidemiological Findings ; II. Elements of Brain Tissue Metabolism; III. Causes and Risk Factors ; Inflammatory System ; Vascular Pathology ; 1. Mitochondrial Dysfunction in AD ; 2. Hypoxia and AD ; 3. History of Stroke, Cerebral Ischemia and AD ; 4. Hypertension and Alzheimer Disease ; Acknowledgments ; References.
Oxidative Stress Induced Mitochondrial Failure and Cellular Hypoperfusion as Primary Pathogenic Factors for the Development and Progression of Alzheimer Disease Abstract ; Introduction ; Cerebral Vascular Energy Requirements: Hypoperfusion as a Key Factor for the Development of AD ; The Effect of Oxidative Stress on Brain Microvessel Function and A<U+00dd> Deposition in AD; Morphometric and Neuropathological Features of CerebroVascular Lesions and A<U+00dd> in AD ; Relationships between ApoE Genotype, Hypercholesterolemia, A<U+00dd> and Vascular Changes in AD.
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