Michael Stuart Brown was born on April 13, 1941, in Brooklyn, New York. In 1962, Brown graduated from the College of Arts and Sciences of the University of Pennsylvania. In 1966, Brown received his M.D. degree from the University of Pennsylvania School of Medicine. For the next two years, Brown was an intern and resident in Internal Medicine at the Massachusetts General Hospital in Boston.
From 1968 to1971, Brown worked at the National Institutes of Health where he served initially as Clinical Associate in gastroenterology and hereditary disease. In 1971, Brown joined the Gastroenterology unit in the Department of Internal Medicine at the University of Texas Southwestern Medical School in Dallas. In 1974, he was promoted to Associate Professor of Internal Medicine at the University of Texas Southwestern Medical School. He became a Professor in 1976. In 1977 he was appointed Paul J. Thomas Professor of Medicine and Genetics, and Director of the Center for Genetic Disease at the same institution. In 1985, Brown was appointed Regental Professor of the University of Texas.
· National Academy of Sciences of the United States (1980)
· American Academy of Arts and Sciences
· American Society for Clinical Investigation
· Association of American Physicians
· American Society of Biological Chemists
· American Society for Cell Biology
· Heinrich Wieland Prize for Research in Lipid Metabolism (1974)
· Lounsbery Award of the U.S. National Academy of Sciences (1979)
· New York Academy of Sciences Award in Biological and Medical Sciences (1981)
· Distinguished Research Award of the Association of American Medical Colleges (1984)
· Research Achievement Award of the American Heart Association (1984)
· William Allan Award of the American Society of Human Genetics (1985)
The following press release from the Royal Swedish Academy of Sciences describes Brown's work:
Michael S. Brown and Joseph L. Goldstein have through their discoveries revolutionized our knowledge about the regulation of cholesterol metabolism and the treatment of diseases caused by abnormally elevated cholesterol levels in the blood. They found that cells on their surfaces have receptors which mediate the uptake of the cholesterol-containing particles called low-density lipoprotein (LDL) that circulate in the blood stream. Brown and Goldstein have discovered that the underlying mechanism to the severe hereditary familial hypercholesterolemia is a complete, or partial, lack of functional LDL-receptors. In normal individuals the uptake of dietary cholesterol inhibits the cells own synthesis of cholesterol. As a consequence the number of LDL-receptors on the cell surface is reduced. This leads to increased levels of cholesterol in the blood which subsequently may accumulate in the wall of arteries causing atherosclerosis and eventually a heart attack or a stroke. Brown and Goldstein's discoveries have lead to new principles for treatment, and prevention, of atherosclerosis.