Tel: (317) 278-3426
Professor M.D. Benson received a B.A. (1961), M.S.- Pathology (1964), and M.D. (1965) from the University of Vermont. He received professional training at Bellevue Hospital (Columbia University College of Physicians and Surgeons) and Boston University.
He joined the faculty of Indiana University in 1976 as Associate Professor of Medicine and became Professor of Medicine in 1981 and Professor of Medical Genetics in 1984.
Professor Benson is an internationally recognized expert in the field of amyloidosis. He has discovered the origin of several forms of hereditary amyloidosis, including those related to mutations in apolipoprotein-A1 and Fibrinogen Aa -chain. His research has revealed structural changes of proteins which are related to the transition of proteins the beta stucture that is characterstic of amyloid fibrils. These studies have included basic research on proteins implicated in amyloidosis of human immunoglobulin (AL), reactive (SAA) and hereditary (TTR) forms of amyloidosis. His research has also lead to significant discoveries in the area of Alzheimer disease, a form of amyloidosis localized to the central nervous system.
Professor Benson was Chairman of the department of Medical and Molecular Genetics from 1996-1999. He is a member of the American Association of Immunologists, American Society of Clinical Investigation, Association of American Professors, American Society of Human Genetics, American Rheumatism Association, the Central Society for Clinical Research, and the International Amyloid Society.
In 2003, The Pasteur-Weizmann Board and the Servier Institute presented in Paris, their prestigious inaugural award, "Pasteur-Weizmann/Servier International Prize in Biomedical Research" to Dr. Benson and his group. This award recognized his pioneering research on "Amyloid" protein deposits. (article link in French)
Dr. Benson and colleagues had also discovered a mutation in the Alzheimer amyloid protein, leading to the development of a widely used mouse model of Alzheimer's disease.