Benjamin Weiss (January 26, 1937) is an American neuropharmacologist, Emeritus Professor of Pharmacology and Physiology at Drexel University College of Medicine. He is best known for his work with cyclic nucleotide phosphodiesterases. He was the first to propose, based on his experimental work, that selective inhibition of phosphodiesterases which are expressed differentially in all tissues, could be used as a target for drug development. His work is the basis for many marketed and developmental human drugs that selectively inhibit cyclic nucleotide phosphodiesterases.
His investigations on the modulation of adrenergic responses in the pineal gland have resulted in the formation of new concepts that may explain the phenomena of drug tolerance and drug hypersensitivity. He and his laboratory were also instrumental in the development of antisense oligonucleotides and antisense RNA as pharmacological tools to study calmodulin and dopamine receptors, and as pharmacological agents for antisense therapy in brain and other tissue.
Early life and education
Weiss was born in The Bronx in 1937 and was raised on a chicken farm in New Jersey where his immigrant parents moved in 1946. Weiss went to Toms River High School, graduating in 1954. He received his undergraduate degree in Pharmacy in 1958 from the Philadelphia College of Pharmacy and Science (now, University of the Sciences), where he also earned a M.Sc. in 1960 and a Ph.D. in Pharmacology in 1963, under the tutelage of G. Victor Rossi. From 1963 to 1966 he had a Postdoctoral Fellowship and a Staff Fellowship at the National Heart Institute, National Institute of Health, where he studied under Bernard B. Brodie. He did further training as a research associate at Columbia University, College of Physicians and Surgeons, with Erminio Costa from 1966 to 1968.
Personal life
In 1959 Weiss married Joyce Zelnick. They have three children and five grandchildren.
Scientific career
From 1968 to 1972 Weiss worked at the National Institute of Mental Health at St Elizabeths Hospital, Washington, D.C., where he held the position of chief of the Section on Neuroendocrinology. In 1972 he accepted the position of professor of pharmacology at the Medical College of Pennsylvania (MCP), where he held the positions of professor of pharmacology and psychiatry, and chief of the Division of Neuropsychopharmacology. He was also a visiting scientist at the Mario Negri Institute for Pharmacological Researchin Milan, Italy, and a visiting scientist at the Weizmann Institute of Science in Rehovot, Israel. On retirement in 1999 he became an emeritus professor in the Department of Pharmacology and Psychiatry at MCP. In 2002, when Drexel University assumed leadership of MCP, he was given the position of professor emeritus in the Department of Pharmacology and Physiology at Drexel University College of Medicine, the position he now holds.
Publications
Weiss is the editor of two books: (Weiss, Benjamin, ed., Cyclic Nucleotides in Disease[1]), and Antisense Oligodeoxynucleotides and Antisense RNA: Novel Pharmacological and Therapeutic Agents[2)). He has also published over 300 scientific articles, reviews and abstracts on his research in molecular biology and molecular pharmacology.
Research
Cyclic Nucleotide Phosphodiesterases:
Weiss and co-workers developed rapid phosphodiesterease assays [3, 4], separated different isozymes of phosphodiesterase in various tissues by electrophoretic methods [5,6]and showed that drugs could selectively inhibit the several isozymes of phosphodiesterase (link) isozymes. He showed that a single cell type may contain more than one form of phosphodiesterase [6,7] and that different forms of phosphodiesterase could be induced or activated by certain neurohormones(e.g. norepinephrine) [7]and intracellular proteins (e.g. calmodulin) [8,9]. He demonstrated that there are different forms of phosphodiesterase in different tissues including the mammalian brain [5,6]and lung [10].
Weiss was the first to show that phosphodiesterase activity is altered in certain disease states [11, 13, 14, 15,16]and to propose that selective inhibition of phosphodiesterase could be the basis of drug selectivity [17,18,19,20]. Weiss and co-workers did extensive work which demonstrated that certain neuropeptides [21,22], alpha adrenergic antagonists [23]and phenothiazineantipsychotic drugs were potent inhibitors of calmodulin activated enzymes [24,25,26,27,28].