Abstract
The pathogenesis of Alzheimer’s disease (AD) is complex, and only a minority of cases appears to be primarily genetic. A relationship between genetic and acquired vascular factors in AD has been hypothesized. Many vascular risk factors for AD, such as atherosclerosis, stroke and cardiac disease in the aging individual, could result in cerebrovascular dysfunction. A major vascular susceptibility factor gene is the apolipoprotein E gene, found to be associated with sporadic late-onset AD cases. Oxidative damage and mitochondrial dysfunction have been also implicated in the pathogenesis of AD, but the question as to whether they are involved in the onset and progression of the pathology or rather represent a consequence of neurodegeneration is still debated. Recent evidence suggests that chronic hypoperfusion may trigger mitochondrial dysfunction in vascular cells which, in turn, may enhance the production of reactive oxygen species. In this short review we revise the link between vascular factors and mitochondrial dysfunction in AD pathogenesis.
Keywords: Alzheimer disease, Ischemia, Mitochondria, mtDNA, Neurodegeneration, Oxidative stress, ROS
Current Neurovascular Research
Title:Vascular Factors and Mitochondrial Dysfunction: a Central Role in the Pathogenesis of Alzheimer’s Disease
Volume: 10 Issue: 1
Author(s): Daniele Orsucci, Michelangelo Mancuso, Elena Caldarazzo Ienco, Costanza Simoncini, Gabriele Siciliano and Ubaldo Bonuccelli
Affiliation:
Keywords: Alzheimer disease, Ischemia, Mitochondria, mtDNA, Neurodegeneration, Oxidative stress, ROS
Abstract: The pathogenesis of Alzheimer’s disease (AD) is complex, and only a minority of cases appears to be primarily genetic. A relationship between genetic and acquired vascular factors in AD has been hypothesized. Many vascular risk factors for AD, such as atherosclerosis, stroke and cardiac disease in the aging individual, could result in cerebrovascular dysfunction. A major vascular susceptibility factor gene is the apolipoprotein E gene, found to be associated with sporadic late-onset AD cases. Oxidative damage and mitochondrial dysfunction have been also implicated in the pathogenesis of AD, but the question as to whether they are involved in the onset and progression of the pathology or rather represent a consequence of neurodegeneration is still debated. Recent evidence suggests that chronic hypoperfusion may trigger mitochondrial dysfunction in vascular cells which, in turn, may enhance the production of reactive oxygen species. In this short review we revise the link between vascular factors and mitochondrial dysfunction in AD pathogenesis.
Export Options
About this article
Cite this article as:
Orsucci Daniele, Mancuso Michelangelo, Caldarazzo Ienco Elena, Simoncini Costanza, Siciliano Gabriele and Bonuccelli Ubaldo, Vascular Factors and Mitochondrial Dysfunction: a Central Role in the Pathogenesis of Alzheimer’s Disease, Current Neurovascular Research 2013; 10 (1) . https://dx.doi.org/10.2174/1567202611310010010
DOI https://dx.doi.org/10.2174/1567202611310010010 |
Print ISSN 1567-2026 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5739 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Transgenic Overproduction of Omega-3 Polyunsaturated Fatty Acids Provides Neuroprotection and Enhances Endogenous Neurogenesis After Stroke
Current Molecular Medicine Uridine Function in the Central Nervous System
Current Topics in Medicinal Chemistry Cellular Senescence as a Target in Cancer Control
Current Cancer Therapy Reviews Acetylcholinesterase Inhibitors as Disease-Modifying Therapies for Alzheimers Disease
Current Medicinal Chemistry Validity of Oxygen-Ozone Therapy as Integrated Medication Form in Chronic Inflammatory Diseases
Cardiovascular & Hematological Disorders-Drug Targets Effect of Withania somnifera Supplementation on Rotenone-Induced Oxidative Damage in Cerebellum and Striatum of the Male Mice Brain
Central Nervous System Agents in Medicinal Chemistry Regulation of Gene Expression by TDP-43 and FUS/TLS in Frontotemporal Lobar Degeneration
Current Alzheimer Research Tau as a Therapeutic Target for Alzheimers Disease
Current Alzheimer Research Migraine, Neurogenic Inflammation, Drug Development - Pharmacochemical Aspects
Current Medicinal Chemistry Influence of Impaired Liver Methionine Metabolism on the Development of Vascular Disease and Inflammation
Current Medicinal Chemistry - Cardiovascular & Hematological Agents The Role of PGC-1α in the Pathogenesis of Neurodegenerative Disorders
Current Drug Targets Polyphenols: A Potential New Strategy for the Prevention and Treatment of Anxiety and Depression
Current Nutrition & Food Science Separation and Purification of Small Peptides from Fermented Sesame Meal and Their Antioxidant Activities
Protein & Peptide Letters Meet Our Editorial Board Member:
Current Drug Safety Endothelium and Oxidative Stress: The Pandora's Box of Cerebral (and Non-Only) Small Vessel Disease?
Current Molecular Medicine Polyunsaturated Fatty Acids and Cardiovascular Disease
Current Pharmaceutical Design The Therapeutic Potential of Melatonin in Neurological Disorders
Recent Patents on Endocrine, Metabolic & Immune Drug Discovery Effects of ACE Inhibitors on Skeletal Muscle
Current Pharmaceutical Design Signal Transduction by the Cytoplasmic Domain of NEUREGULIN-1 and its Roles During Neuronal Aging
Current Signal Transduction Therapy Diagnoses of Pathological States Based on Acetylcholinesterase and Butyrylcholinesterase
Current Medicinal Chemistry