Raymond Swanson, MD
|Title||Professor in Residence|
|School||UCSF School of Medicine|
|Address||4150 Clement Street|
San Francisco CA 94143
Raymond A. Swanson, M.D. is a graduate of the University of Michigan Medical School and the University of California, San Francisco Neurology Residency training program. He is currently Chief of the Neurology and Rehabilitation Service at the San Francisco Veterans Affairs Medical Center. Dr. Swanson has a longstanding interest in brain bioenergetics, and current studies focus on the intersection of oxidative stress, mitochondria, and neuronal death.
A current focus of his work is the ubiquitous nuclear enzyme, poly(ADP-ribose polymerase-1 (PARP-1). PARP-1 is normally functions in DNA repair, but which also mediates bioenergetic failure during excitotoxic and oxidative cell death. PARP activation is also an important mediator of microglial activation, by virtue of its interaction with the transcription factor NF-kB. One aim of his work is to elucidate the bioenergetic events between activation of PARP and cell death under disease conditions in brain. A related question concerns the cellular origin of oxidative stress that activates PARP-1. Oxidant production in neurons is widely attributed to the mitochondria, but superoxide is produced by NADPH oxidase in response to neuronal NMDA receptor activation. This superoxide signal normally contributes to synaptic remodeling, but it can also produce oxidative stress and cell death. He is now working to identify key regulatory steps in the signaling pathways linking NMDA receptors to NADPH oxidase function. Importantly, NADPH oxidase requires glucose to regenerate NADPH substrate, thus forming another intriguing link to cell bioenergetics. A second source of oxidative stress is impaired oxidant scavenging. He has identified the “glutamate” transporter EAAT3 as the major route of neuronal cysteine uptake. Mice that lack EAAT3 have reduced glutathione levels in neurons and undergo age-dependent neurodegeneration and cognitive impairment. The dopaminergic neurons of the substantia nigra are particularly affected. These studies are germane to Parkinson’s disease, ischemia, and other conditions in which oxidative stress contributes to neuronal demise.
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