Abstract
Accumulation of DNA damage and impairment of DNA repair systems are involved in the pathogenesis of different neurodegenerative diseases. Whenever DNA damage is too extensive, the DNA damage response pathway provides for triggering cellular senescence and/or apoptosis. However, whether the increased level of DNA damage in neurodegenerative disorders is a cause rather than the consequence of neurodegenerative events remains to be established. Among possible DNA lesions, DNA double strand breaks (DSBs) are rare events, nevertheless they are the most lethal form of DNA damage. In neurons, DSBs are particularly deleterious because of their reduced DNA repair capability as compared to proliferating cells.
Here, we provide a description of DSB repair systems and describe human studies showing the presence of several types of DNA lesions in three major neurodegenerative diseases including Alzheimer’s disease (AD), Parkinson’s disease (PD) and Huntington’s disease (HD). Then, we analyze the role of DSB accumulation and deficiency of DSB repair systems in neurodegeneration by examining studies on animal models of neurodegenerative diseases.
Keywords: Alzheimer's disease, DNA damage, DNA repair, DNA double strand breaks, Huntington's disease, neurodegenerative diseases, Parkinson's disease.
Current Alzheimer Research
Title:DNA Double Strand Breaks: A Common Theme in Neurodegenerative Diseases
Volume: 13 Issue: 11
Author(s): Daniela Merlo, Cristiana Mollinari, Mauro Racaniello, Enrico Garaci and Alessio Cardinale
Affiliation:
Keywords: Alzheimer's disease, DNA damage, DNA repair, DNA double strand breaks, Huntington's disease, neurodegenerative diseases, Parkinson's disease.
Abstract: Accumulation of DNA damage and impairment of DNA repair systems are involved in the pathogenesis of different neurodegenerative diseases. Whenever DNA damage is too extensive, the DNA damage response pathway provides for triggering cellular senescence and/or apoptosis. However, whether the increased level of DNA damage in neurodegenerative disorders is a cause rather than the consequence of neurodegenerative events remains to be established. Among possible DNA lesions, DNA double strand breaks (DSBs) are rare events, nevertheless they are the most lethal form of DNA damage. In neurons, DSBs are particularly deleterious because of their reduced DNA repair capability as compared to proliferating cells.
Here, we provide a description of DSB repair systems and describe human studies showing the presence of several types of DNA lesions in three major neurodegenerative diseases including Alzheimer’s disease (AD), Parkinson’s disease (PD) and Huntington’s disease (HD). Then, we analyze the role of DSB accumulation and deficiency of DSB repair systems in neurodegeneration by examining studies on animal models of neurodegenerative diseases.
Export Options
About this article
Cite this article as:
Merlo Daniela, Mollinari Cristiana, Racaniello Mauro, Garaci Enrico and Cardinale Alessio, DNA Double Strand Breaks: A Common Theme in Neurodegenerative Diseases, Current Alzheimer Research 2016; 13 (11) . https://dx.doi.org/10.2174/1567205013666160401114915
DOI https://dx.doi.org/10.2174/1567205013666160401114915 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
Call for Papers in Thematic Issues
New Advances in the Prevention, Diagnosis, Treatment, and Rehabilitation of Alzheimer's Disease
Aims and Scope: Introduction: Alzheimer's disease (AD) poses a significant global health challenge, with an increasing prevalence that demands concerted efforts to advance our understanding and strategies for prevention, diagnosis, treatment, and rehabilitation. This thematic issue aims to bring together cutting-edge research and innovative approaches from multidisciplinary perspectives to address ...read more
Current updates on the Role of Neuroinflammation in Neurodegenerative Disorders
Neuroinflammation is an invariable hallmark of chronic and acute neurodegenerative disorders and has long been considered a potential drug target for Alzheimer?s disease (AD) and dementia. Significant evidence of inflammatory processes as a feature of AD is provided by the presence of inflammatory markers in plasma, CSF and postmortem brain ...read more
Deep Learning for Advancing Alzheimer's Disease Research
Alzheimer's disease (AD) poses a significant global health challenge, with an increasing number of individuals affected yearly. Deep learning, a subfield of artificial intelligence, has shown immense potential in various domains, including healthcare. This thematic issue of Current Alzheimer Research explores the application of deep learning techniques in advancing our ...read more
Diagnostic and therapeutic biomarkers of dementia
Dementia affects 18 million people worldwide. Dementia is a syndrome of symptoms caused by brain disease, usually chronic or progressive, clinically characterized by multiple impairments of higher cortical functions such as memory, thinking, orientation, and learning. In addition, in the course of dementia, cognitive deficits are observed, which often hinder ...read more
- 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
- Announcements
Related Articles
-
Alpha-1-Adrenergic Receptor Blockade Modifies Insulin-Regulated Aminopeptidase (IRAP) Activity in Rat Prostate and Modulates Oxytocin Functions
Drug Metabolism Letters The Potential of Microalgae for the Production of Bioactive Molecules of Pharmaceutical Interest
Current Pharmaceutical Biotechnology JAK Inhibitors: Pharmacology and Clinical Activity in Chronic Myeloprolipherative Neoplasms
Current Medicinal Chemistry Bcl-2 Family Proteins as Therapeutic Targets
Current Pharmaceutical Design T Cell Costimulatory and Inhibitory Receptors as Therapeutic Targets for Inducing Anti-Tumor Immunity
Current Cancer Drug Targets A Current Review of Cypermethrin-Induced Neurotoxicity and Nigrostriatal Dopaminergic Neurodegeneration
Current Neuropharmacology Can Tea Consumption be a Safe and Effective Therapy Against Diabetes Mellitus-Induced Neurodegeneration?
Current Neuropharmacology Role of PARP Inhibitors in Cancer Biology and Therapy
Current Medicinal Chemistry The Role of Autophagy in the Pathogenesis of Ischemic Stroke
Current Neuropharmacology Subtype Selectivity in Phosphodiesterase 4 (PDE4): A Bottleneck in Rational Drug Design
Current Pharmaceutical Design RNA Therapeutics Directed to the Non Coding Regions of APP mRNA, In Vivo Anti-Amyloid Efficacy of Paroxetine, Erythromycin, and N-acetyl cysteine
Current Alzheimer Research Cancer/Testis Antigens Trigger Epithelial-Mesenchymal Transition and Genesis of Cancer Stem-Like Cells
Current Pharmaceutical Design Peroxisome Proliferator Activated Receptor-Gamma Ligands as Potent Antineoplastic Agents
Current Medicinal Chemistry - Anti-Cancer Agents The use of Azoles Containing Natural Products in Cancer Prevention and Treatment: An Overview
Anti-Cancer Agents in Medicinal Chemistry Serum Starvation Induces BACE1 Processing and Secretion
Current Alzheimer Research Targeted Angiogenesis Therapy in Head and Neck Squamous Cell Carcinomas
Current Angiogenesis (Discontinued) Activation of Human Platelets by 2-Arachidonoylglycerol: Role of PKC in NO/cGMP Pathway Modulation
Current Neurovascular Research Targeting IGF-I, IGFBPs and IGF-I Receptor System in Cancer: The Current and Future in Breast Cancer Therapy
Recent Patents on Anti-Cancer Drug Discovery MRP1-dependent Collateral Sensitivity of Multidrug-resistant Cancer Cells: Identifying Selective Modulators Inducing Cellular Glutathione Depletion
Current Medicinal Chemistry Endocannabinoids as Regulators of Transient Receptor Potential (TRP)Channels: a Further Opportunity to Develop New Endocannabinoid-Based Therapeutic Drugs
Current Medicinal Chemistry