Mutations in several genes associated with early onset Alzheimer’s result in increased extracellular concentrations of the longer form of the beta-amyloid peptide Ab 1-42 relative to Ab 1-40. It is this longer form of Ab that has been shown to be toxic to neurons and may serve as a catalyst for the aggregation and deposition of Ab to produce the neurotoxic effects associated with senile plaque formation. Using the Ab peptide in a yeast two-hybrid screen, a novel interacting protein designated the endoplasmic reticulum-associated amyloid beta-peptide-binding protein (ERAB)/L-3-hydroxyacyl-CoA dehydrogenase type II has been identified. It is shown to be expressed at high levels in Alzheimer’s disease-affected brain. ERAB may contribute to neuronal dysfunction in Alzheimer’s disease.
HSD17B10; hydroxysteroid (17-beta) dehydrogenase 10; HADH2, hydroxyacyl Coenzyme A dehydrogenase, type II, hydroxyacyl Coenzyme A dehydrogenase, type II , mental retardation, X linked, syndromic 10 , MRXS10; 3-hydroxyacyl-CoA dehydrogenase type-2; 17b HSD10; AB binding alcohol dehydrogenase; ABAD; CAMR; ERAB; MHBD; MRPP2; SDR5C1; short chain dehydrogenase/reductase family 5C; member 1; type 10 17b HSD; type 10 17beta hydroxysteroid dehydrogenase; AB-binding alcohol dehydrogenase; mitochondrial ribonuclease P protein 2; 3-hydroxy-2-methylbutyryl-CoA dehydrogenase; short chain type dehydrogenase/reductase XH98G2; amyloid-beta peptide binding alcohol dehydrogenase; short chain L-3-hydroxyacyl-CoA dehydrogenase type 2; short chain dehydrogenase/reductase family 5C, member 1; endoplasmic reticulum-associated amyloid beta-peptide-binding protein; HCD2; HADH2; MRX17; MRX31; SCHAD; MRXS10; 17b-HSD10; DUPXp11.22; im:6899159; wu:fj61f03; zgc:101605; hydroxyacyl-Coenzyme A dehydrogenase, type II