Therapeutic Intervention at the Gene Level to Ameliorate Neurodegenerative Diseases Using Small Molecules

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Dr. Zawia’s group is focused on drug discovery/development for neurodegenerative diseases. Dr. Zawia is continuing his work from the USA related to the identification of a novel class of mechanism-based drugs for the treatment of neurodegenerative diseases, such as Alzheimer’s disease (AD), Progressive Supranuclear Palsy (PSP), and Frontotemporal Dementia (FTD). He had repurposed a lead drug tolfenamic acid as an investigational drug for the treatment of PSP currently under final approval for a human trial at the US FDA. Derivatives of this lead compound are currently under preclinical development at QBRI.

Latest Publications

  • J Hill, NH Zawia (2021). Fenamates as Potential Therapeutics for Neurodegenerative Disorders, Cells 10, 702.
  • A Leso, SW Bihaqi, A Masoud, JK Chang, A Lahouel, N Zawia (2019). Loss in efficacy measures of tolfenamic acid in a tau knock-out model: Relevance to Alzheimer’s disease Experimental Biology and Medicine, 1535370219871249.
  • JK Chang, A Leso, GM Subaiea, A Lahouel, A Masoud, F Mushtaq, ... NH Zawia (2018). Tolfenamic Acid: A Modifier of the Tau Protein and its Role in Cognition and Tauopathy, Current Alzheimer Research 15 (7), 655-663.
  • A Eid, SW Bihaqi, WE Renehan, NH Zawia (2016). Developmental Lead (Pb) Exposure and Lifespan Alterations in Epigenetic Regulators and their Correspondence to Biomarkers of Alzheimer’s Disease. Journal of Alzheimer’s and Dementia DADM, 2, 123-131.
  • GM Subaiea, AH Ahmed, LI Adwan, NH Zawia (2015). Reduction of Amyloid-β Deposition and Attenuation of Memory Deficits by Tolfenamic Acid. J Alzheimers Dis.;43(2):425-33.
  • GM Subaiea, BH Alansi, DA Serra, M Alwan, NH Zawia (2011). 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.
  • LI Adwan, R Basha, M Abdelrahim, GM Subaiea, NH Zawia (2011). 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.