- Dean of the Graduate School and Professor
- Office: 395F Lab: 380
- Phone: 401.874.5368
- Email: email@example.com
- Office Location: 7 Greenhouse Road, Kingston, RI 02881
Dr. Zawia’s research deals with two aspects: the latent effects of environmental insults on the developing brain, and discovery of a novel class of mechanism-based drugs for the treatment of Alzheimer’s disease (AD). His research group focuses on lead (Pb) as a model environmental hazard to which early-life exposure reprograms gene expression impacting the neurodegenerative process in the aging brain.
His group has provided the first basic science evidence of the role of epigenetic pathways and factors in mediating latent effects on disease due to developmental exposure, and in doing so have generated the first evidence for the developmental origins of Alzheimer’s disease. In addition to exploring environmental risk factors for neurodegenerative diseases, the lab has repurposed a novel class of mechanism-based drugs for the treatment of AD, of which a lead drug tolfenamic acid is under consideration for clinical trials.
Environmental risk factors for Alzheimer’s disease; Pinpointing potential biomarkers for Alzheimer’s disease; Developing drugs for the treatment of neurodegenerative diseases
Post-doc, National Institutes of Health (NIEHS), 1994
Ph.D., University of California, Irvine, CA,1989
M.S., Loma Linda University, Loma Linda, CA, 1986
B.S., University of Massachusetts, Amherst, MA, 1984
Sankpal UT, Lee CM, Connelly SF, Kayaleh O, Eslin D, Sutphin R, Goodison S, Adwan L, Zawia NH, Lichtenberger LM, Basha R.Cellular and organismal toxicity of the anti-cancer small molecule, tolfenamic acid: a pre-clinical evaluation. Cell Physiol Biochem. 32(3):675-86, 2013.
Bihaqi SW, ZawiaNH.Enhanced taupathy and AD-like pathology in aged primate brains decades after infantile exposure to lead (Pb).Neurotoxicology. 39:95-101, 2013.
Bihaqi SW, Bahmani A, Subaiea GM, Zawia NH. Infantile exposure to lead and late-age cognitive decline: Relevance to AD. Alzheimers Dement. doi:pii: S1552-5260(13)00131-3. 10.1016/j.jalz.2013.02.012. [Epub ahead of print]
Subaiea GM, Adwan LI, Ahmed AH, Stevens KE, Zawia NH. Short-term treatment with tolfenamic acid improves cognitive functions in Alzheimer’s disease mice. Neurobiol Aging. 34(10):2421-30, 2013.
Adwan L, Zawia NH. Epigenetics: a novel therapeutic approach for the treatment of Alzheimer’s disease. Pharmacol Ther. 139(1):41-50, 2013.
Dosunmu, R, Alashwal, H, Zawia, NH. Genome-wide expression and methylation profiling in the aged rodent brain due to early-life Pb exposure and its relevance to aging. Mech Ageing Dev. 2012 May 18. [Epub ahead of print]
Bihaqi, SW, Schumacher, A, Maloney, B, Zhang, Y, Lahiri, DK, Zawia, NH. Do epigenetic pathways initiate late onset Alzheimer disease (LOAD): towards a new paradigm. Curr Alzheimer Res. Current Alzheimer Research 9, 577-591 (2012).
Bihaqi, SW, Huang, H, Wu, J, Zawia, NH. Infant exposure to lead (Pb) and epigenetic modifications in the aging primate brain: implications for Alzheimer’s disease. J Alzheimers Dis. 27(4):819-33 (2011).
Subaiea, GM, Alansi, BH, Serra, DA, Alwan, M, Zawia. NH. The ability of tolfenamic acid to penetrate the brain: a model for testing the brain disposition of candidate Alzheimer’s drugs using multiple platforms. Curr Alzheimer Res. 8(8):860-7 (2011).
Adwan, LI, Basha, R, Abdelrahim, M, Subaiea, GM, Zawia, NH. Tolfenamic acid interrupts the de novo synthesis of the _-amyloid precursor protein and lowers amyloid beta via a transcriptional pathway. Curr Alzheimer Res. 8(4): 385-92 (2011).
Huang, H, Bihaqi, SW, Cui, L, Zawia, NH. In vitro Pb exposure disturbs the balance between A_ production and elimination: the role of A_PP and neprilysin. Neurotoxicology 32(3):300-6 (2011).
Zawia, NH, et al. Epigenetics, oxidative stress and Alzheimer disease. Free Radical Biology & Medicine 46:1241-1249 (2009).
Lahiri, DK, Maloney, B, Zawia. NH. The LEARn model: an epigenetic explanation for idiopathic neurobiological disease. Molecular Psychiatry. Nature Publishing Group. 14:992-1003 (2009).