Gal Bitan

Gal Bitan

Professor-in-Residence

Neurology

University of California Los Angeles, USA

About the Speaker:

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.

Selected Recent Publications:

1. Dutta S, Hornung S, Taha HB, Bitan G (2023) Biomarkers for parkinsonian disorders in CNS-originating EVs: promise and challenges. Acta Neuropathol 145:515-540.

2. Taha HB, Hornung S, Dutta S, Fenwick L, Lahgui O, Howe K, Elabed N, Del Rosario I, Wong DY, Duarte Folle A, Markovic D, Palma JA, Kang UJ, Alcalay RN, Sklerov M, Kaufmann H, Fogel BL, Bronstein JM, Ritz B, Bitan G (2023) Toward a biomarker panel measured in CNS-originating extracellular vesicles for improved differential diagnosis of Parkinson's disease and multiple system atrophy. Transl Neurodegener 12:14

3. Palma JA, Martinez J, Millar Vernetti P, Ma T, Perez MA, Zhong J, Qian Y, Dutta S, Maina KN, Siddique I, Bitan G, Ades-Aron B, Shepherd TM, Kang UJ, Kaufmann H (2022) mTOR Inhibition with Sirolimus in Multiple System Atrophy: A Randomized, Double-Blind, Placebo-Controlled Futility Trial and 1-Year Biomarker Longitudinal Analysis. Mov Disord 37:778-789.

4. Dutta S, Hornung S, Kruayatidee A, Maina KN, Del Rosario I, Paul KC, Wong DY, Duarte Folle A, Markovic D, Palma JA, Serrano GE, Adler CH, Perlman SL, Poon WW, Kang UJ, Alcalay RN, Sklerov M, Gylys KH, Kaufmann H, Fogel BL, Bronstein JM, Ritz B, Bitan G (2021) α-Synuclein in blood exosomes immunoprecipitated using neuronal and oligodendroglial markers distinguishes Parkinson's disease from multiple system atrophy. Acta Neuropathol 142:495-511.

5. Di J, Siddique I, Li Z, Malki G, Hornung S, Dutta S, Hurst I, Ishaaya E, Wang A, Tu S, Boghos A, Ericsson I, Klärner FG, Schrader T, Bitan G (2021) The molecular tweezer CLR01 improves behavioral deficits and reduces tau pathology in P301S-tau transgenic mice. Alzheimers Res Ther 13:6.