ABAD: a potential therapeutic target for Abeta-induced mitochondrial dysfunction in Alzheimer's disease

A T Marques; P A Fernandes; M J Ramos

doi:10.2174/138955709788681627

ABAD: a potential therapeutic target for Abeta-induced mitochondrial dysfunction in Alzheimer's disease

Mini Rev Med Chem. 2009 Jul;9(8):1002-8. doi: 10.2174/138955709788681627.

Authors

A T Marques¹, P A Fernandes, M J Ramos

Affiliation

¹ REQUIMTE, Departamento de Química, Faculdade de Ci ências, Universidade do Porto, Rua do Campo Alegre, 687, 4169-007 Porto, Portugal.

PMID: 19601895
DOI: 10.2174/138955709788681627

Abstract

Amyloid-beta-peptide (Abetabinding to mitochondrial Abeta-binding alcohol dehydrogenase (ABAD) enzyme triggers a series of events leading to mitochondrial dysfunction characteristic of Alzheimer's 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-Abeta interaction, namely structural and biophysical data, available inhibitors and more recent data from proteomic studies.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

3-Hydroxyacyl CoA Dehydrogenases / antagonists & inhibitors
3-Hydroxyacyl CoA Dehydrogenases / chemistry*
3-Hydroxyacyl CoA Dehydrogenases / genetics
3-Hydroxyacyl CoA Dehydrogenases / metabolism*
Alzheimer Disease / enzymology*
Alzheimer Disease / physiopathology
Amyloid beta-Peptides / chemistry
Amyloid beta-Peptides / metabolism*
Animals
Humans
Mitochondria / pathology
Models, Molecular

Substances

Amyloid beta-Peptides
3-Hydroxyacyl CoA Dehydrogenases
HSD17B10 protein, human