Gal Bitan completed his graduate studies in organic chemistry at the Hebrew University of Jerusalem, Israel. Dr. Bitan's graduate work on unnatural amino acids and non-conventional peptide cyclization methodologies led him to postdoctoral studies on the structural biology of bone-related ligand-receptor systems including integrins and G protein-coupled receptors at Clark University, Worcester, MA and Beth Israel-Deaconess Medical Center/Harvard Medical School, Boston, MA. Dr. Bitan then moved on to tackle the problem of protein misfolding and aggregation, which is 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. In Alzheimer's disease, the amyloid β-protein (Aβ) self-associates to form a variety of oligomeric and polymeric structures with potent neurotoxic activities. In particular, Aβ oligomers have been implicated as the probable cause of Alzheimer's disease. For example, Aβ oligomers have been found in brains of Alzheimer's disease patients but not in those of age-matched healthy individuals. Dr. Bitan introduced the use of novel photochemical protein cross-linking techniques for investigation of Aβ assembly and discovered one of the earliest oligomers in the assembly cascade, the paranucleus. In 2003, Dr. Bitan was appointed as an Instructor in Neurology in the Center for Neurologic Disease at Brigham and Women's Hospital and Harvard Medical School. In 2004, Dr. Bitan joined UCLA where he is currently an Assistant Professor of Neurology in the David Geffen School of Medicine. In recognition of his achievements, in 2005, Dr. Bitan received the Turken research award for the study of Alzheimer's disease.