Dr. Bari specializes in the neurosurgical repair and restoration of brain and nerve function. Following his neurosurgery residency training at UCLA, Dr. Bari was awarded the prestigious William P. Van Wagenen Fellowship to train at the world-renowned functional neurosurgery program at the University of Toronto. He has extensive clinical and research experience in the use of deep brain stimulation (DBS) in the treatment of both movement and psychiatric disorders. Dr. Bari’s clinical practice includes DBS surgery for Parkinson’s disease, tremor, dystonia, depression and OCD. In addition, his clinical practice includes neurosurgery for brain tumors, pain, and peripheral nerve disorders.
Dr. Bari’s research focuses on an interdisciplinary approach to studying the neurobiology underlying movement and psychiatric disorders and expanding the frontiers of neurosurgery to treat those disorders. As a part of his fellowship training, Dr. Bari studied the relationship between the motor and reward systems of the brain and the use of deep brain stimulation to modify and enhance them. A native of California, Dr. Bari completed his neurosurgery residency training at UCLA after receiving his MD and PhD degrees from Boston University. He completed his undergraduate training at UC Berkeley in the field of neurobiology.
Gal Bitan got his PhD in organic chemistry from 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 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 devastating diseases, such as 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 ß-protein (Aß) self-associates to form a variety of oligomeric and polymeric structures with potent neurotoxic activities. In particular, Aß oligomers have been implicated as the probable cause of Alzheimer’s disease. Dr. Bitan introduced the use of novel photochemical protein cross-linking techniques for investigation of Aß assembly and discovered one of the earliest oligomers in the assembly cascade, the paranucleus. In 2004, Dr. Bitan joined UCLA where he is currently a Professor of Neurology. His research program is focused on translational science geared at developing novel, mechanism-based diagnostic and therapeutic tools for neurodegenerative diseases, including Alzheimer’s disease and other tauopathies, Parkinson’s disease, multiple system atrophy, and amyotrophic lateral sclerosis.