Abstract
Amyloid-beta-peptide (Aβ) binding to mitochondrial Aβ-binding alcohol dehydrogenase (ABAD) enzyme triggers a series of events leading to mitochondrial dysfunction characteristic of Alzheimers disease (AD). Thus this interaction may represent a novel target for treatment strategy against AD. In this review we summarize current findings regarding the ABAD-Aβ interaction, namely structural and biophysical data, available inhibitors and more recent data from proteomic studies.
Keywords: ABAD, Alzheimer's disease, amyloid-β, mitochondrial dysfunction, neuronal cell death, oxidative stress, frentizole, AG18051 inhibitor
Mini-Reviews in Medicinal Chemistry
Title: ABAD: A Potential Therapeutic Target for Aβ-Induced Mitochondrial Dysfunction in Alzheimers Disease
Volume: 9 Issue: 8
Author(s): A. T. Marques, P. A. Fernandes and M. J. Ramos
Affiliation:
Keywords: ABAD, Alzheimer's disease, amyloid-β, mitochondrial dysfunction, neuronal cell death, oxidative stress, frentizole, AG18051 inhibitor
Abstract: Amyloid-beta-peptide (Aβ) binding to mitochondrial Aβ-binding alcohol dehydrogenase (ABAD) enzyme triggers a series of events leading to mitochondrial dysfunction characteristic of Alzheimers disease (AD). Thus this interaction may represent a novel target for treatment strategy against AD. In this review we summarize current findings regarding the ABAD-Aβ interaction, namely structural and biophysical data, available inhibitors and more recent data from proteomic studies.
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Cite this article as:
Marques T. A., Fernandes A. P. and Ramos J. M., ABAD: A Potential Therapeutic Target for Aβ-Induced Mitochondrial Dysfunction in Alzheimers Disease, Mini-Reviews in Medicinal Chemistry 2009; 9 (8) . https://dx.doi.org/10.2174/138955709788681627
DOI https://dx.doi.org/10.2174/138955709788681627 |
Print ISSN 1389-5575 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5607 |
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