ABAD: a potential therapeutic target for Abeta-induced mitochondrial dysfunction in Alzheimer's disease.
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.
Marques
A T
AT
REQUIMTE, Departamento de Química, Faculdade de Ci ências, Universidade do Porto, Rua do Campo Alegre, 687, 4169-007 Porto, Portugal.
Fernandes
P A
PA
Ramos
M J
MJ
D015094:3-Hydroxyacyl CoA Dehydrogenases / Q000037:antagonists & inhibitors / Q000737:chemistry* / Q000235:genetics / Q000378:metabolism*; D000544:Alzheimer Disease / Q000201:enzymology* / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000737:chemistry / Q000378:metabolism*; D000818:Animals; D006801:Humans; D008928:Mitochondria / Q000473:pathology; D008958:Models, Molecular
D016229:Amyloid beta-Peptides; D015094:3-Hydroxyacyl CoA Dehydrogenases; C108634:HSD17B10 protein, human