Amyloid beta-binding alcohol dehydrogenase (ABAD)

Amyloid beta-binding alcohol dehydrogenase is a mitochondrial enzyme belonging to the short-chain dehydrogenase/reductase family. It is also known as 17β-hydroxysteroid dehydrogenase type 10. This enzyme has a broad substrate specificity, including roles in steroid metabolism and energy regulation within mitochondria. Critically, it binds amyloid-beta peptide with high affinity; this interaction exacerbates amyloid-beta-induced oxidative stress, impairs mitochondrial function, and contributes to neuronal dysfunction observed in Alzheimer's disease. Inhibition of the ABAD–amyloid-beta interaction—using small molecules or decoy peptides—has been shown to protect against these pathological effects in preclinical models by improving mitochondrial activity, reducing oxidative damage, enhancing degradation of amyloid-beta within mitochondria, and improving cognitive performance. As such, ABAD represents an emerging therapeutic target for neurodegenerative diseases characterized by amyloid pathology.

Other names

ABADAβ-binding alcohol dehydrogenase17β-hydroxysteroid dehydrogenase type 10 (HSD10)

Inhibitors block the interaction between ABAD and amyloid-beta, reducing mitochondrial dysfunction and neuronal toxicity associated with Alzheimer’s disease.