Nigel H. Greig, Ph.D.
Translational Gerontology Branch
251 Bayview Boulevard
Baltimore, MD 21224
The Drug Design and Development Section (DDDS) is designed to identify drugs that improve brain function and/or forestall the neurodegenerative process in age-related neurodegenerative disorders. Data arising from studies on neurodegenerative and neuroprotective signaling pathways are used to identify potential drug targets. Candidate drugs are first screened for efficacy in cell culture or animal models, and the most effective compounds are moved through preclinical studies to clinical trials. Several drugs that enhance cognitive function are currently in clinical trials, and novel neuroprotective compounds are at various preclinical stages of development.
Nigel Greig was trained as a pharmacologist with a background in medicinal chemistry and physiology and gained his Ph.D. from the University of London; specifically, from the Pharmacology Department of the Royal College of Surgeons, England. Leaving the Cancer Chemotherapy Department of the Imperial Cancer Research Fund, London, he joined NIA in 1982. His initial studies focused on optimizing the delivery to and action of drugs within the brain. This resulted in the development of drug candidates for the treatment of brain tumors, and cancers of the breast, lymphatics and ovaries, as well as agents for the treatment of drug abuse and technology for the delivery of neuropeptides, antisense oligonucleotides and proteins to the brain. Leaving NIA in 1989, Dr. Greig was involved in the initiation of the successful California biotechnology company, Athena Neurosciences, now Elan Pharmaceuticals.The company was launched on technology from Dr. Greig's program. Returning to NIA as a tenured scientist in 1991, his research has evolved into his present interest, the design and development of drugs and diagnostics for the treatment of neurodegenerative diseases, with particular emphasis on Alzheimer's disease, and of type 2 diabetes. He heads the Drug Design and Development Section of the Laboratory of Neurosciences that extensively collaborates within NIA, academia and industry. This has resulted in the development of several agents from concept in the laboratory, through the required U.S. Government regulatory requirements to the bedside. Patents covering a variety of novel compounds of clinical interest have now been licensed from the NIA to industry and are in preclinical and clinical development, and new research within his program is providing both publications and patent applications to support potential drugs of the future.
Chen S, Yu SJ, Li Y, Lecca D, Glotfelty E, Kim HK, Choi HI, Hoffer BJ, Greig NH, Kim DS, Wang Y. Post-treatment with PT302, a long-acting Exendin-4 sustained release formulation, reduces dopaminergic neurodegeneration in a 6-Hydroxydopamine rat model of Parkinson's disease. Sci Rep. 2018;8(1):10722.
Athauda D, Maclagan K, Skene SS, Bajwa-Joseph M, Letchford D, Chowdhury K, Hibbert S, Budnik N, Zampedri L, Dickson J, Li Y, Aviles-Olmos I, Warner TT, Limousin P, Lees AJ, Greig NH, Tebbs S, Foltynie T. Exenatide once weekly versus placebo in Parkinson's disease: a randomised, double-blind, placebo-controlled trial. Lancet. 2017;390(10103):1664-1675.
Becker RE, Seeman MV, Greig NH, Lahiri DK. What can triumphs and tribulations from drug research in Alzheimer's disease tell us about the development of psychotropic drugs in general? Lancet Psychiatry. 2015;2(8):756-764.
Maccecchini ML, Chang MY, Pan C, John V, Zetterberg H, Greig NH. Posiphen as a candidate drug to lower CSF amyloid precursor protein, amyloid-β peptide and τ levels: target engagement, tolerability and pharmacokinetics in humans. J Neurol Neurosurg Psychiatry. 2012;83(9):894-902.
Tweedie D, Ferguson RA, Fishman K, Frankola KA, Van Praag H, Holloway HW, Luo W, Li Y, Caracciolo L, Russo I, Barlati S, Ray B, Lahiri DK, Bosetti F, Greig NH, Rosi S. Tumor necrosis factor-α synthesis inhibitor 3,6'-dithiothalidomide attenuates markers of inflammation, Alzheimer pathology and behavioral deficits in animal models of neuroinflammation and Alzheimer's disease. J Neuroinflammation. 2012;9:106.
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This page was last updated on August 21st, 2018