Prof. Eli Heldman
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Professor Emeritus
Department :
Clinical Biochemistry and Pharmacology
Room :
316
בנין כימיה וטכנולוגיה כימית, 3
Phone :
972-8-6461976
972-8-6461977
972-8-6477675
Email :
heldmane@bgu.ac.il
Office Hours :
Education
Postdoctoral 1973 1975, National Institutes of Health, NHLBI, Bethesda Maryland, Laboratory of Biochemical Genetics (Mentor: Dr. Marshal Nirenberg).
Ph.D. 1970 1973, City University of New York Department of Biochemistry (Mentor: Prof. Walter Essman).
M.Sc. 1967 1968, Hadassah Medical School of the Hebrew University of Jerusalem, Department of Cellular Biochemistry (Mentor: Prof. Jacob Mager). Technion 1966, Institute of Technology, Department of Chemistry, complementary studies in chemistry. (Mentor: Prof. Ruth Ben-Yishai).
B.Sc. 1962 1965, The Hebrew University of Jerusalem, Faculty of Agriculture.
Research Interests
Much of the research is related to neurodegenerative diseases, in particular Alzheimer’s and Parkinson’s disease and drug delivery with relevance to these diseases. 1) Alzheimer’s disease: Beta-amyloid is believed to be a major toxic element involved in the pathogenesis of Alzheimer’s disease. We investigate the transduction pathways that mediate the processing of the Alzheimer’s amyloid precursor protein (APP) and pathways that lead to the formation of the pathological beta-amyloid. We found that the processing of APP by alpha-secretase is mediated by at least two transduction pathways, PKC-dependent pathway and MAPP kinase-dependent pathway. We are trying to identify, within these pathways, targets for novel drugs for the treatment of Alzheimer's disease. The aim is to find drugs that will shift the processing of the precursor protein to the non-amyloidogenic pathway and thus will reduce the formation of the pathological beta-amyloid. 2) In addition, we investigate the mechanism of beta-amyloid toxicity. The production of reactive oxygen species by beta amyloid and their possible contribution to neurotoxicity are being investigated. We found that exposue of cells to beta-amyloid reduces the level of intracellular free thiols and that neurotrophic factors such as NGF protects against beta-amyloid toxicity 3) Parkinson’s disease: A major problem in the treatment of Parkinson’s disease is the late motor complications, the development of which is believed to be accelerated by the intermittent stimulation of the dopaminergic receptors due to the intervallic nature od levodopa administration (the oral administration of L-DOPA is the most common and effective treatment). The mechanisms underlying the deleterious effects of the intermittent receptor stimulation is unknown. We are investigating how various dopaminergic treatment regimens affect the transduction pathways of the dopaminergic receptors, and thus, may lead to the development of the late motor complications. We focus on adenylyl cyclase activity, the enzyme which is directly affected by the G protein coupled to the dopaminergic receptors. We are developing novel ways for delivering a continuous (rather than intermittent) administration of L-DOPA and thereby increase their efficacy. We invented a novel transdermal delivery system of levodopa (US patent #6,166,081 from December 26, 2000), which is now being developed commercially for the treatment of Parkinson’s disease. 4) Neurodegeneration: We investigate the mechanism by which potentially pathogenic factors (e.g. beta-amyloid, oxidative stress) cause neurodegeneration (death of nerve cells) and we are trying to identify targets for drugs that will demonstrate neuroprotection features. 5) Drug delivery: We are developing novel and unique vesicles, based on a natural oil from Vernonia galamensis for delivering drugs to the brain through the blood-brain barrier. These are stable nano-size vesicles that due to their unique surfaces loose their stability only at the target site and release the treating drug at its site of action. In addition, we develop transdermal delivery system of L-DOPA for the treatment of Parkinson's disease.