Gal Bitan, Ph.D.
Gal Bitan at:
Gal Bitan received his B.Sc. in Chemistry and Biochemistry in 1988, and M.Sc. in Organic Chemistry in 1989 from the Hebrew University of Jerusalem, Israel. He went on to pursue graduate studies in Organic Chemistry at the Hebrew University and received his Ph.D. in 1996. His graduate research was dedicated to developing new methods for the synthesis of unnatural amino acids and their utilization to create unconventional cyclic peptides for use in medicine. His patented inventions provided the core technology for the start-up company Peptor, Inc. Peptor was acquired later by AndromedA Biotech, which makes DiaPep277, an FDA-approved drug for type I diabetes. Dr. Bitan went on to pursue postdoctoral studies on the structural biology of ligand-receptor systems at Harvard Medical School/Beth Israel-Deaconess Medical Center and continued to tackling the problem of protein misfolding and aggregation at Harvard Medical School/Brigham and Women's Hospital, where he became an Instructor of Neurology in 2003.
As a postdoctoral fellow and then an Instructor, Dr. Bitan made fundamental contributions to the study of early events in the pathologic cascades that cause Alzheimer's disease. Working with David Teplow, he introduced the use of the novel photochemical protein cross-linking technique, PICUP, for investigation of amyloid β-protein (Aβ) assembly and discovered one of the earliest oligomers in the assembly cascade, the paranucleus. The use of PICUP helped explain how Aβ forms toxic oligomers, the differences in toxicity among the two major Aβ forms - Aβ40 and Aβ42, and the structure-activity relationships in mutant forms of Aβ linked to familial Alzheimer's disease.
In 2004, Dr. Bitan joined the Department of Neurology in the David Geffen School of Medicine at UCLA where he is currently a Professor. His research program is dedicated to developing new therapeutic and diagnostic tools for neurodegenerative diseases and a better understanding of the process of abnormal protein aggregation, which underlies over 30 diseases. The abnormal aggregation leads to formation of toxic oligomers and amyloid fibrils that disrupt cellular function and communication, and ultimately causes cell death. Each disease is characterized by the abnormal self-association of certain proteins that affect particularly vulnerable cells and/or organs. For example, in Alzheimer's disease, the proteins Aβ and tau gradually destroy the hippocampus and certain cortical regions in the brain. To mitigate the harmful action of the toxic protein oligomers and aggregates, Dr. Bitan's laboratory has been using diverse strategies, including testing inhibitors and modulators of protein–protein interaction in vitro, in cell culture, and in animal models. Diagnostic tools are developed using human serum and plasma samples obtained from multiple clinics and biobanks.
Dr. Bitan has published more than 90 original research articles, 26 chapters, and 13 reviews. He occasionally contributes commentaries to Alzforum and other media outlets. He serves as a reviewer for many scientific journals, NIH and VA study sections and other funding agencies, and as a member of the editorial boards of several journals, including Journal of Biological Chemistry, Frontiers in Molecular Neuroscience, Scientific Reports, Annals of Translational Medicine, Biomolecules, and Pharmacogenomics and Personalized Medicine. He is also a member of the scientific advisory boards of the American Federation for Aging Research, Give to Cure, and KalGene Therapeutics, Inc.