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Dr. Taw​feeq Shekh-Ahmad | Center for Nanoscience and Nanotechnology

Dr. Taw​feeq Shekh-Ahmad

tawfeek s
Dr.
Taw​feeq
Shekh-Ahmad
School of Pharmacy, Institute for Drug Research

Brief Summary of research: 

we investigate the processes and sources that contribute to the generation of free radicals and reactive oxygen species that lead to oxidative stress, and its relation with pathophysiological functions in CNS disorders, mainly in epileptogenesis (the process by which brain injury leads to chronic epilepsy) and established epilepsy. We aim to develop antioxidant therapies centered around the multiple neuroprotective effects of the nuclear factor erythroid 2-related factor 2 (Nrf2), described as the "master regulator" of the anti-oxidant response. In addition, we study novel gene therapy approaches that will be implemented in different rodent models, target genes and genetic approaches, to develop antioxidant gene therapy for targeting oxidative stress in CNS diseases.

Specific research topics related to Nanoscience and Nanotechnology:

Within the recent years, I have acquired a great interest in implementing polymeric nanosystems and lipid nanoparticulate as delivery strategies for existing and newly developed potential CNS therapies. 

The use of traditional drugs loaded in innovative nano-carriers for prolonged and controlled release systems could reduce the number of drug administrations, increase the protection from seizures, decrease side effects associated with conventional drugs, and thus improve the treatment of epilepsy and other CNS diseases.

In addition, we are looking at delivery of viral and non-viral vectors capable of transducing target cells while avoiding impact on non-target cells. Non-viral vectors, which are essentially DNA-containing nanoparticles, can be retargeted by incorporating ligands into their lipid or protein shells, but to date there are no convincing studies to demonstrate the in vivo utility of retargeted non-viral vectors.
We aim to develop a non-viral gene delivery encoding antioxidant genes and/or peptides that inhibit production of ROS, to drive the expression in the main cell type responsible for the generation of ROS.