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