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.
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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 |
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