An intracellular protein that binds amyloid-β peptide and mediates neurotoxicity in Alzheimer's disease

Shi Du Yan (), Jin Fu, Claudio Soto, Xi Chen, Huaijie Zhu, Futwan Al-Mohanna, Kate Collison, Aiping Zhu, Eric Stern, Takaomi Saido, Masaya Tohyama, Satoshi Ogawa, Alex Roher and David Stern
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Shi Du Yan: Surgery and Physiology, and Cellular Biophysics, Columbia Unversity, College of Physicians and Surgeons
Jin Fu: Surgery and Physiology, and Cellular Biophysics, Columbia Unversity, College of Physicians and Surgeons
Claudio Soto: New York University Medical Center
Xi Chen: Surgery and Physiology, and Cellular Biophysics, Columbia Unversity, College of Physicians and Surgeons
Huaijie Zhu: Surgery and Physiology, and Cellular Biophysics, Columbia Unversity, College of Physicians and Surgeons
Futwan Al-Mohanna: Biological and Medical Research, King Faisal Specialist Hospital and Research Centre
Kate Collison: Biological and Medical Research, King Faisal Specialist Hospital and Research Centre
Aiping Zhu: Surgery and Physiology, and Cellular Biophysics, Columbia Unversity, College of Physicians and Surgeons
Eric Stern: Surgery and Physiology, and Cellular Biophysics, Columbia Unversity, College of Physicians and Surgeons
Takaomi Saido: Tokyo Metropolitan Institute of Medical Science
Masaya Tohyama: Osaka University Medical School
Satoshi Ogawa: Osaka University Medical School
Alex Roher: Haldeman Laboratory for Alzheimer's Disease Research, Sun Health Research Institute
David Stern: Surgery and Physiology, and Cellular Biophysics, Columbia Unversity, College of Physicians and Surgeons

Nature, 1997, vol. 389, issue 6652, 689-695

Abstract: Abstract Amyloid-β is a neurotoxic peptide which is implicated in the pathogenesis of Alzheimer's disease. It binds an intracellular polypeptide known as ERAB, thought to be a hydroxysteroid dehydrogenase enzyme, which is expressed in normal tissues, but is overexpressed in neurons affected in Alzheimer's disease. ERAB immunoprecipitates with amyloid-β, and when cell cultures are exposed to amyloid-β, ERAB inside the cell is rapidly redistributed to the plasma membrane. The toxic effect of amyloid-β on these cells is prevented by blocking ERAB and is enhanced by overexpression of ERAB. By interacting with intracellular amyloid-β, ERAB may therefore contribute to the neuronal dysfunction associated with Alzheimer's disease.

Date: 1997
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DOI: 10.1038/39522

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