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
-
Cannabinoid System in Neurodegeneration: New Perspectives in Alzheimers Disease
Mini-Reviews in Medicinal Chemistry Microbial Agents, Immune Function and Atheromatosis: The Chlamydophila pneumoniae Role
Current Immunology Reviews (Discontinued) Retraction Notice to Role of Vitamin K2 in the Treatment of Postmenopausal Osteoporosis
Current Drug Safety Editorial (Thematic Issue: Neuroglia as a Central Element of Neurological Diseases: An Underappreciated Target for Therapeutic Intervention)
Current Neuropharmacology Rexinoids as Therapeutics for Alzheimer’s Disease: Role of APOE
Current Topics in Medicinal Chemistry The Effect of TNFα-Inhibitors on Cardiovascular Events in Patients with Rheumatoid Arthritis: An Updated Systematic Review of the Literature
Current Rheumatology Reviews Aging and DNA Methylation
Current Chemical Biology The Double Roles of the Prostaglandin E<sub>2</sub> EP2 Receptor in Intracerebral Hemorrhage
Current Drug Targets Secondary Hypertension: The Ways of Management
Current Vascular Pharmacology Cognitive Dysfunction in FMR1 Premutation Carriers
Current Psychiatry Reviews From Bitopic Inhibitors to Multitarget Drugs for the Future Treatment of Alzheimer’s Disease
Current Medicinal Chemistry The Role of Endothelin-1 in Obstructive Sleep Apnea Syndrome and Pulmonary Arterial Hypertension: Pathogenesis and Endothelin-1 Antagonists
Current Medicinal Chemistry Biological Signatures of Alzheimer’s Disease
Current Topics in Medicinal Chemistry Novel Therapeutic Strategies in Major Depression: Focus on RNAi and Ketamine
Current Pharmaceutical Design Design, Synthesis and Characterization of Novel Urolithin Derivatives as Cholinesterase Inhibitor Agents
Letters in Drug Design & Discovery The Role of Physical Exercise and Omega-3 Fatty Acids in Depressive Illness in the Elderly
Current Neuropharmacology Distinctive Effects of Aerobic and Resistance Exercise Modes on Neurocognitive and Biochemical Changes in Individuals with Mild Cognitive Impairment
Current Alzheimer Research Inflammation-Mediating Proteases: Structure, Function in (Patho) Physiology and Inhibition
Protein & Peptide Letters Caveolin-1 in Stroke Neuropathology and Neuroprotection: A Novel Molecular Therapeutic Target for Ischemic-Related Injury
Current Vascular Pharmacology BACE1 Deficient Mice: Their Role in Drug Target Validation and Implications for Alzheimers Disease Therapies
Current Medicinal Chemistry - Immunology, Endocrine & Metabolic Agents