Abstract
Current strategies for the treatment of Alzheimer’s disease (AD) involve tackling the formation or clearance of the amyloid-beta peptide (Aβ) and/or hyper-phosphorylated tau, or the support and stabilization of the remaining neuronal networks. However, as we gain a clearer idea of the large number of molecular mechanisms at work in this disease, it is becoming clearer that the treatment of AD should take a combined approach of dealing with several aspects of the pathology. The concept that we also need to protect specific sensitive targets within the cell should also be considered. In particular the role of protecting the function of a specific mitochondrial protein, amyloid binding alcohol dehydrogenase (ABAD), will be the focus of this review. Mitochondrial dysfunction is a well-recognized fact in the progression of AD, though until recently the mechanisms involved could only be loosely labeled as changes in ‘metabolism’. The discovery that Aβ can be present within the mitochondria and specifically bind to ABAD, has opened up a new area of AD research. Here we review the evidence that the prevention of Aβ binding to ABAD is a drug target for the treatment of AD.
Keywords: ABAD, mitochondria, Alzheimer’s disease, and drug discovery
Current Alzheimer Research
Title:Is Amyloid Binding Alcohol Dehydrogenase a Drug Target for Treating Alzheimer’s Disease?
Volume: 10 Issue: 1
Author(s): Eva Borger, Laura Aitken, Heng Du, Wenshen Zhang, Frank J Gunn-Moore and Shirley Shi Du Yan
Affiliation:
Keywords: ABAD, mitochondria, Alzheimer’s disease, and drug discovery
Abstract: Current strategies for the treatment of Alzheimer’s disease (AD) involve tackling the formation or clearance of the amyloid-beta peptide (Aβ) and/or hyper-phosphorylated tau, or the support and stabilization of the remaining neuronal networks. However, as we gain a clearer idea of the large number of molecular mechanisms at work in this disease, it is becoming clearer that the treatment of AD should take a combined approach of dealing with several aspects of the pathology. The concept that we also need to protect specific sensitive targets within the cell should also be considered. In particular the role of protecting the function of a specific mitochondrial protein, amyloid binding alcohol dehydrogenase (ABAD), will be the focus of this review. Mitochondrial dysfunction is a well-recognized fact in the progression of AD, though until recently the mechanisms involved could only be loosely labeled as changes in ‘metabolism’. The discovery that Aβ can be present within the mitochondria and specifically bind to ABAD, has opened up a new area of AD research. Here we review the evidence that the prevention of Aβ binding to ABAD is a drug target for the treatment of AD.
Export Options
About this article
Cite this article as:
Borger Eva, Aitken Laura, Du Heng, Zhang Wenshen, J Gunn-Moore Frank and Shi Du Yan Shirley, Is Amyloid Binding Alcohol Dehydrogenase a Drug Target for Treating Alzheimer’s Disease?, Current Alzheimer Research 2013; 10 (1) . https://dx.doi.org/10.2174/1567205011310010004
DOI https://dx.doi.org/10.2174/1567205011310010004 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
- 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
-
Efficacy and Toxicity of Clioquinol Treatment and A-beta42 Inoculation in the APP/PSI Mouse Model of Alzheimer's Disease
Current Alzheimer Research Coated with Nanomaterials Intraocular Lenses, Ophthalmic and Human Body Implantable Devices with High Catalytic Antioxidant Activities: A New Nanotechnology Strategy of Peroxidase Cellular Enzyme Mimics Increasing the Biocompatibility and Therapeutic Deployment of the Medical Prosthetic Device
Recent Patents on Drug Delivery & Formulation Anderson-Fabry Disease: A Multiorgan Disease
Current Pharmaceutical Design Ribosome-inactivating Proteins from Root Tubers and Seeds of Trichosan-thes kirilowii and Other Trichosanthes Species
Protein & Peptide Letters Emotion, Decision-Making and Substance Dependence: A Somatic-Marker Model of Addiction
Current Neuropharmacology TNF-α and IL-8 in Acute Stroke and the Modulation of these Cytokines by Antiplatelet Agents
Current Neurovascular Research Cooling the Injured Brain: How Does Moderate Hypothermia Influence the Pathophysiology of Traumatic Brain Injury
Current Pharmaceutical Design Vascular Oxidative Stress: A Key Factor in the Development of Hypertension Associated with Ethanol Consumption
Current Hypertension Reviews Targeting the p53 Pathway of Apoptosis
Current Pharmaceutical Design Potential Role of (-)-Epigallocatechin-3-Gallate (EGCG) in the Secondary Prevention of Alzheimer Disease
Current Drug Targets Expression and Function of Cytokines and Chemokines in Neuropsychiatric Related Systemic Lupus Erythematosus
Current Rheumatology Reviews Management of the Menopausal Disturbances and Oxidative Stress
Current Pharmaceutical Design The Role of Inflammation in Neurological Disorders
Current Pharmaceutical Design Electroacupuncture Reduces Hemiplegia Following Acute Middle Cerebral Artery Infarction with Alteration of Serum NSE, S-100B and Endothelin
Current Neurovascular Research Physiological Role of Peroxisome Proliferator-Activated Receptors Type Alpha on Dopamine Systems
CNS & Neurological Disorders - Drug Targets Molecular Mechanisms, Proteinopathies and Therapeutic Strategies in Neurodegenerative Disorders
Current Genomics Editorial [Hot Topic: Innate Immune Responses in CNS Neurodegenerative Diseases (Guest Editors: Hans van Noort and Sandra Amor)]
CNS & Neurological Disorders - Drug Targets Ascorbic Acid: Its Role in Immune System and Chronic Inflammation Diseases
Mini-Reviews in Medicinal Chemistry Tumor Necrosis Factor-α-Mediated Pulmonary Endothelial Barrier Dysfunction
Current Respiratory Medicine Reviews Transient Opening of the Blood-Brain Barrier by Vasoactive Peptides to Increase CNS Drug Delivery: Reality Versus Wishful Thinking?
Current Neuropharmacology