The Bukhari lab studies the brain circuitry and physiology of a rare brain disorder called dystonia. Dystonia is an involuntary movement disorder manifested by abnormal body postures that lead to permanent disability. There is currently no disease-modifying therapy, a major unmet clinical need. We would like to thank dystonia patients and healthy volunteers who have participated in our research studies.
Your time and dedication are the hope and key to our success. If you would like to learn more about our work, please email us at email@example.com.
The Bukhari lab maintains a culture of respect, pride and inclusion for all members of our community.
The Bukhari Lab studies the brain circuitry and physiology of a rare brain disorder called dystonia.
Dystonia is an involuntary movement disorder manifested by abnormal body postures that lead to permanent disability. There is currently no disease modifying therapy, a major unmet clinical need.
One of the key mechanisms of dystonia is an alteration of synaptic plasticity, a mechanism for learning and memory. The Bukhari Lab seeks to understand the disruption of synaptic plasticity in brain circuitry of human dystonia. This abnormality was previously reported to occur in deep brain regions in mouse models of dystonia. However, due to limitation in technology, the abnormality in synaptic plasticity has only been studied at the superficial cortical brain regions in human dystonia. At the Bukhari Lab, we have developed advanced technology to evaluate the mechanism of abnormal plasticity in deep brain regions in human dystonia. We use a non-invasive brain stimulation technology called transcranial magnetic stimulation (TMS) to understand the brain circuit of dystonia patients and measure changes in functional brain networks and its effect on clinical measures of dystonia.
A second goal of our research is to use insights gained from our evaluation of the abnormal plasticity mechanism in human dystonia to develop a long-lasting clinical therapy. To this end, we are applying advanced functional neuroimaging approaches and computational modeling to precisely deliver a TMS stimulation paradigm informed by biological understanding of the disease and change the abnormal neural circuitry in dystonia. Our goal is to identify a brain stimulation approach and pattern that can rectify the abnormal brain plasticity in human dystonia and provide long lasting clinical benefit for patients.
Collectively, the mechanistic and therapeutic goals of our research study have significant benefit for advancing the care of dystonia patients. Understanding the disease mechanism will inform the development of future clinical therapies for all dystonia patients. TMS is FDA approved for treatment of depression, migraine and obsessive-compulsive disorder. Demonstrating therapeutic benefit in human dystonia will provide a novel, and non-invasive clinical therapy for dystonia patients.
• Bukhari, Noreen, Poromendro N. Burman, Ayan Hussein, Michael P. Demars, Masato Sadahiro, Daniel M. Brady, Stella E. Tsirka, Scott J. Russo, and Hirofumi Morishita. “Unmasking Proteolytic Activity for Adult Visual Cortex Plasticity by the Removal of Lynx1.” J Neurosci 35, no. 37 (September 16, 2015): 12693–702. https://doi.org/10.1523/JNEUROSCI.4315-14.2015.
• Bukhari, Noreen, Luisa Torres, John K. Robinson, and Stella E. Tsirka. “Axonal regrowth after spinal cord injury via chondroitinase and the tissue plasminogen activator (tPA)/plasmin system.” J Neurosci 31, no. 42 (October 19, 2011): 14931–43. https://doi.org/10.1523/JNEUROSCI.3339-11.2011.
• Nolin, Westley B., Jaime Emmetsberger, Noreen Bukhari, Yan Zhang, Joel M. Levine, and Stella E. Tsirka. “tPA-mediated generation of plasmin is catalyzed by the proteoglycan NG2.” Glia 56, no. 2 (January 15, 2008): 177–89. https://doi.org/10.1002/glia.20603.
• Olszewski, Rafal T., Noreen Bukhari, Jia Zhou, Alan P. Kozikowski, Jarda T. Wroblewski, Susan Shamimi-Noori, Barbara Wroblewska, et al. “NAAG peptidase inhibition reduces locomotor activity and some stereotypes in the PCP model of schizophrenia via group II mGluR.” J Neurochem 89, no. 4 (May 2004): 876–85. https://doi.org/10.1111/j.1471-4159.2004.02358.x.
• Bacich, Dean J., Epolia Ramadan, Denise S. O’Keefe, Noreen Bukhari, Iga Wegorzewska, Olumide Ojeifo, Rafal Olszewski, et al. “Deletion of the glutamate carboxypeptidase II gene in mice reveals a second enzyme activity that hydrolyzes N-acetylaspartylglutamate.” J Neurochem 83, no. 1 (October 2002): 20–29. https://doi.org/10.1046/j.1471-4159.2002.01117.x.
The Bukhari lab is always looking for interested, talented members for our research team. Please email Dr. Bukhari at firstname.lastname@example.org to learn more about open positions.
Current position: Medical student, Georgetown University School of Medicine
Current position: Completing Duke undergraduate in Mathematics and Computer Science
Current Position: Clinical Research Coordinator at Veteran Affairs Portland Health Care System
Current Position: Senior Clinical Research Coordinator at Infectious Disease Division, Duke Internal Medicine Department
Current position: Completing Master's degree in statistics, Duke University