John H. Weiss
The information listed below is current as of the date the transcript was finalized.
Abstract of Interview
John H. Weiss grew up in San Francisco, California, the oldest of three children. His parents were both psychiatrists. He attended a private grade school and a less traditional high school; he found school interesting but not especially difficult. He developed his interest in math and science early, and he found that science came naturally to him as he was interested in discerning patterns in the way the world works. Weiss entered Stanford University, where he majored in biology with a focus on neuroscience. After taking an extra year of undergraduate study, he applied to medical school. He spent six months in a biochemistry research lab, and he attended science classes while at Stanford University School of Medicine, but uncertainty prevented Weiss from seeking a lab position. He found that the practical challenges of medical residency proved more difficult than course work when he started a neurology residency. During that residency he met Dennis W. Choi and entered the Stanford PhD program in neuroscience. In the Choi lab he began work on mechanisms of nerve cell degeneration in stroke and on glutamate's toxic effect on nerve cells. Choi proposed two phases of glutamate injury. Research on nerve degenerative diseases on Guam led Weiss to study β-N-methylamino-L-alanine (BMAA). His work in the Choi lab on BMAA yielded clues regarding AMPA/kainate receptor activation in nerve-degenerative diseases. He discovered that BMAA's toxicity depends on a covalent interaction with other compounds, explaining about AMPA/kainate toxicity and receptor activation, the role of voltage-sensitive calcium channels, BMAA's role in nerve-degenerative disease, and the finding that zinc accumulation in voltage-sensitive calcium channels might cause cell death (apoptosis). Weiss accepted a position at University of California, Irvine, and received a Pew Scholars Program in the Biomedical Sciences award and a National Institutes of Health grant, though he did not have lab space immediately available at Irvine. While starting his lab he had teaching and clinical responsibilities, he had to find and hire postdocs, and he had to mentor students. At the end of the interview Weiss discusses AMPA/kainate-type glutamate receptor-mediated toxicity in selective nerve cell degeneration; calcium in selective injury; a collaboration with the Choi lab to study "cobalt positive" NADPH-diaphorase cells; attempts to improve upon historically poor results of calcium imaging studies; correlating calcium influx and intercellular calcium levels with cell death; and the role of zinc in selective injury. His collaboration with Carl Cotman on β-amyloid protein's toxicity in cortical cell cultures and new directions for research on cellular functions constituted his attempts to establish a reputation separate from Choi's and to overcome the competitive pressure he felt in his field. He concludes by saying that he has found a supportive community at the Pew Scholars Program in the Biomedical Sciences annual meetings.
Stanford University Hospital
University of California, Irvine
|1980 to 1981||
Stanford Medical Alumni Scholar
|1980 to 1981||
March of Dimes Medical Student Research Fellowship
|1987 to 1990||
American Academy of Neurobiology Research Fellowship in Neuropharmacology
|1990 to 1991||
Dana Fellow in Neuroscience
|1990 to 1995||
National Institute on Aging Clinician Investigator Award
|1992 to 1996||
Pew Scholar in the Biomedical Sciences
Table of Contents
Family background. Parents' nontraditional values and psychoanalytic training. Early schooling. Attends an alternative high school in San Francisco during theearly 1970s. Develops a social conscience. Early interest in math and science. Interest in discerning patterns in how the world works. Stanford University. Declares a major in biology with a focus on neuroscience. Father'spsychoanalytic career and its impact on Weiss's research focus. Takes an extrayear of undergraduate study. Undergraduate life.
Applies to medical school. Six-month stint in a biochemistry research lab. Attends science classes while at Stanford University School of Medicine. Practical challenges of medical residency. Neurology residency and meeting Dennis W. Choi. Enters the Stanford PhD program in neuroscience. Lack ofleisure time as a medical student. Work on mechanisms of nerve celldegeneration in stroke. Research on glutamate's toxic effect on nerve cells. Crucial role of N-methyl-D-aspartate (NMDA) receptors. Advantages of using cell culture systems rather than whole-animal models. Preference for theory-driven science over technique-driven. Interest in doing basic research rather than applied. University of California, Irvine's Institute for Brain Aging andDementia. Research on nerve degenerative diseases on Guam leads to study of ß-N-methylamino-L-alanine (BMAA). AMPA/kainate receptor activation in nerve-degenerative diseases. AMPA/kainate toxicity and receptor activation. Role of voltage-sensitive calcium channels. Zinc accumulation in voltage-sensitive calcium channels may cause cell death.
University of California, Irvine. Pew Scholars Program in the Biomedical Sciences and National Institutes of Health grants. Teaching and clinical responsibilities. Postdocs. Hong Zhen Yin. Mentoring students. AMPAkainite-type glutamate receptor-mediated toxicity in selective nerve cell degeneration. Role of calcium in selective injury. Collaboration with the Choi lab to study "cobalt positive" NADPH-diaphorase cells. Correlating calciuminflux and intercellular calcium levels with cell death. Carl W. Cotman and ß-amyloid protein's toxicity in cortical cell cultures. Hannah Monyer.
Broad research questions. Belief that basic research with clear clinical reference will continue to be funded. Science funding. Pew annual meetings.