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Moussa B. H. Youdim is an internationally renowned Israeli neuroscientist specializing in neurochemistry and neuropharmacology. He is the discoverer of both monoamine oxidase (MAO) B inhibitors l-deprenyl (Selegiline) and rasagiline (Azilect) as anti-Parkinson drugs which possess neuroprotective activities. He is currently professor emeritus at Technion - Faculty of Medicine and President of Youdim Pharmaceuticals.
Youdim was born in Tehran, Iran second of five children. His father worked and traded with the British and wanted that the boys to be educated in England. He and his brother were sent to England boarding school in UK. He had an ambition to go to medical school to study medicine and obtained his preclinical studies in Borough Polytechnique in London. he was accepted at McGill University in Montreal where he aobtained his B.Sc. degree. A lecture in neurochemsitry changed his mind about medical degree and decided to study brain chemistry.
Youdim upon joining Professor Theodore L Sourkes's laboratory at Allan Memorial Institute, McGill Department of Psychiatry, he began to work on the M.Sc. focusing on characteristics of the enzume monoamine oixdase (MAO), followed by Ph.D. He has focused most of his life on the field of neurochemistry and neuropharmacology of aminergic neurotransmitters in health and disease. In his M.Sc. and Ph.D. Studies he purified mitochondrial MAO and demonstrated two forms of the enzymes, which were later named A and B by Johnson ( 1968). One of his most important contributions to science was working with Professor Merton Sandler in London University Post Graduate School to study MAO inhibitors as anti-depressants and anti-Parkinson drugs. While at Oxford University Medical School, a chance meeting with Professor Peter Riederer resulted in employing the MAO-B inhibitor, l-deprenyl (Later named selegiline) a failed anti depressant, in Parkinson's disease, since the human brain basal ganglia were rich in MAO-B and dopamine. The clinical study was a success and was confirmed by others in clinical studies and eventual approval of selegiline by FDA.
At Technion in Haifa he discovered the second MAO B inhibitor, AGN1135, which was 20 times more potent than selegiline. Together with Prof. John Finberg and Teva Pharmecueitacl AGN1135 was developed as an anti Parkinson's Disease drug called rasagiline (Azilect), approved by FDA in 2006. This drug had neuroprotective activity in cell culture and in vivo animal models of Parkinson's disease and may have disease modifying activity in Parkinson's disease.
He pioneered the study of brain iron dysregulation on brain function. This included its nutritional deficiency, which results in cognitive impairment and learning process in animal models and children with nutritional iron deficiency. And iron accumulation in brain neurons that degenerate resulting in Parkinson's and Alzheimer's diseases and ALS (amyotropic lateral sclerosis), where iron initiated oxidative stress may induce the process neurodegeneration. He was the first to demonstrate that iron chelators su desferal and VK-28 were neuroprotective in animal models of Parkinson's disease since neurodegeneration of substantia nigra dopamine neuros results in accumulation of iron. Free iron may cause generation of free radicals and oxidative stress. His other pioneering contribution is the development of multi-target drugs for treatment of Parkinson's and Alzheimer's diseases possessing iron chleating, monomaine oxidase and cholinesterase inhibitory activities
Youdim has published almost nine hundred papers and reviews and edited 45 books in neurochemistry, neuropharmacology, multi-target drug development, and transcriptomics.
Youdim served as consultant to Roche, TEVA Pharmaceuticals Ltd; Ciba Geigy, and Continental Pharmaceuticals, Brussels. He is president and CSO of Youdim Pharmaceutical. He is a discoverer of the anti-Parkinson drugs selelgiline (l-deprenyl) and developer of monoamine oxidase B inhibitor rasagiline (Azilect), which was considered to be the first disease modifying drug used for Parkinson's disease and TVP 3326, ladostigil, for Alzheimer's disease.[2][3] Experts have recently questioned whether rasagiline actually has significant disease modifying properties.[4]
On the editorial boards of 40 journals, including British Journal of Pharmacology, Journal of Neurochemistry, Journal of Neural Transmission, Experimental Neurology, International Neurochemistry, Psychopharmacology. International Journal of Neuropsychopharmacology, Archives of Pharmacology, Frontiers in Pharmacology, European Journal of Pharmacology, Biogenic Amines, Neuropsychobiology, Neurochemical Research; Brain Research, CNS Drug Review, Future Drugs, Drugs of Today, and Neurotherapeutics.