Modeling neurological and psychiatric diseases with human stem cells

by Rusty Gage

• President of the Salk Institute
• head of the Laboratory of Genetics at the Salk Institute for Biological Studies
• Vi and John Adler Chair for Research on Age-Related Neurodegenerative Diseases
• Adjunct Professor in the Department of Neurosciences, UCSD

Biography

Fred H. Gage, Ph.D. received his Ph.D. in 1976 from The Johns Hopkins University. Dr. Gage’s work concentrates on the adult central nervous system and unexpected plasticity and adaptability to environmental stimulation that remains throughout the life of all mammals. In addition, he models human neurological and psychiatric disease in vitro using human stem cells. Finally his lab studies the genomic mosaicism that exists in the brain as a result of mobile elements that are active during neurogenesis.

He has won numerous prizes and awards for his work including the the Keio Medical Science Prize, the IPSEN Prize for Neuroplasticity, the Charles A. Dana Award, and the Metropolitan Life Research Award. He serves on many health-related boards and was President of the Society for Neuroscience and the International Society for Stem Cell Research. He is a a Member of the National Academy of Sciences and the National Academy of Medicine, a Fellow of the American Association for the Advancement of Science, a Member of the American Academy of Arts and Sciences, an Associate Member of the European Molecular Biology Organization, and a member of the American Philosophical Society.

iMM, Lisbon

Mitochondria at the synapse have a pivotal role in neurotransmitter release, but almost nothing is known about synaptic mitochondria composition or specific functions. Synaptic mitochondria compared to mitochondria in other cells, need to cope with increased calcium load, more oxidative stress, and high demands of energy generation during synaptic activity. We aim to unravel how synaptic mitochondria have learnt to adapt to this environment, and how the disruption of these acquired mechanisms contributes to neurodegeneration.

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