ABAD: A Potential Therapeutic Target for Aβ-Induced Mitochondrial Dysfunction in Alzheimers Disease

Author(s): A. T. Marques, P. A. Fernandes, M. J. Ramos

Journal Name: Mini-Reviews in Medicinal Chemistry

Volume 9 , Issue 8 , 2009

Become EABM
Become Reviewer


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

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2009
Page: [1002 - 1008]
Pages: 7
DOI: 10.2174/138955709788681627
Price: $65

Article Metrics

PDF: 5