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Gerald D. Fischbach MD
Dr. Fischbach joined the Simons Foundation in early 2006 to oversee the Simons Foundation Autism Research Initiative. Formerly Dean of the Faculties of Health Sciences at Columbia University, and former Director of the National Institute of Neurological Disorders and Stroke at the N.I.H. from 1998-2001, Dr. Fischbach received his M.D. degree in 1965 from Cornell University Medical School and interned at the University of Washington Hospital in Seattle. He began his research career at the National Institutes of Health, serving from 1966 – 1973. He subsequently served on the faculty of Harvard Medical School, first as Associate Professor of Pharmacology from 1973 – 1978 and then as Professor until 1981. From 1981 – 1990, Dr. Fischbach was the Edison Professor of Neurobiology and Head of the Department of Anatomy and Neurobiology at Washington University School of Medicine. In 1990, he returned to Harvard Medical School where he was the Nathan Marsh Pusey Professor of Neurobiology and Chairman of the Neurobiology Departments of Harvard Medical School and Massachusetts General Hospital until 1998. Throughout his career, Dr. Fischbach has studied the formation and maintenance of synapses, the contacts between nerve cells and their targets through which information is transferred in the nervous system. He pioneered the use of nerve cell cultures to study the electrophysiology, morphology, and biochemistry of developing nerve – muscle and inter-neuronal synapses. His current research is focused on roles that neurotrophic factors play in determination of neural precursor fate, synapse formation, and neuronal survival. Dr. Fischbach is a past-President of the Society of Neuroscience and serves on several medical and scientific advisory boards. He is a member of the National Academy of Sciences, the American Academy of Arts and Science, the Institute of Medicine, and a fellow of the American Association for the Advancement of Science and a non-resident Fellow of the Salk Institute.
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Written by Gerald D. Fischbach
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Copyright 2008 © Simons Foundation
The field of human genetics continues to advance at an increasing rate so this bill is long overdue. The implications extend beyond health insurance to matters of subtile social discrimination and career opportunities. Most common diseases are due to complex interactions between many genes that enhance or diminish risk rather than cause or prevent a particular disorder. Public scrutiny may lead to oversimplification of this complex web, to the detriment of the individual.
The genetics bill sets a valuable precedent for other areas of biomedical science. As techniques of brain imaging improve and as cognitive scientists refine questions that can be posed to normal and diseased brains, structural and functional images must remain private.
For every clinical intervention, one must weigh risks and benefits. The enormous benefits of the MMR vaccine are there for all to see. The risks are minimal. No accepted epidemiological study to date has linked preservatives in the vaccine to autism. Senator McCain is wrong. After many years in which science has been sidelined in Washington, we must hope that a higher level of scientific discourse will emerge as the presidential campaign unfolds. We all have an obligation to learn and to inform others and to help those in positions of responsibility.
Neuropsychiatric disorders were defined based on an astute clinical observation more than half a century ago. Molecular analyses seem now to be showing that certain facets of such disorders may share common mechanisms. Is the cognitive deficit in schizophrenia different on a molecular or circuit level than the cognitive deficit in autism? In any case, we must consider that the same genetic lesions may be involved in both. It may be a quantitative issue - more or less gene expression rather than a yes or no matter. Deletions in autism and duplications in schizophrenia of the same piece of DNA is an astounding finding!
The contactin binding protein shown to be mutated in several cases of autism is a member of the neurexin family. This adds to the list of autism risk factors including other neurexins, neuroligins and shank 3, that help organize the molecular machinery at synapses.
Each mutation is, apparently, a rare event, but in the aggregate they may point to common pathways. How might other proteins that affect synaptic function, formation, plasticity or loss be assayed?