Gal Bitan completed his graduate studies in organic chemistry at the Hebrew University of Jerusalem, Israel. His graduate work on unnatural amino acids and nonconventional peptide cyclization methodologies led him to postdoctoral studies on the structural biology of ligand-receptor systems at Clark University, Worcester, MA and Beth Israel-Deaconess Medical Center/Harvard Medical School, Boston, MA, followed by a second postdoc in which he entered the field of abnormal protein folding and aggregation—a process involved in over 30 amyloid-related diseases including Alzheimer's disease, Parkinson's disease, prion diseases (e.g., mad cow disease), amyotrophic lateral sclerosis (Lou Gherig's disease), and type II diabetes. Working at Brigham and Women’s Hospital/Harvard Medical School, Boston, MA, Dr. Bitan has made fundamental contributions to the study of early events in the pathologic cascades that cause Alzheimer's disease. Dr. Bitan introduced the use of novel photochemical protein cross-linking techniques for investigation of Amyloid β-protein (Aβ) assembly, and discovered one of the earliest oligomers in the assembly cascade, the paranucleus. In 2004, Dr. Bitan joined UCLA where he is currently an Associate Professor of Neurology in the David Geffen School of Medicine. His research program focuses on deciphering the molecular interactions underlying aberrant protein folding assembly and on developing novel compounds to prevent the toxicity of protein aggregates as therapeutic tools for diseases associated with protein aggregation, including Alzheimer's and Parkinson's diseases.
Biography Updated on 3 April 2012