Abdelhamid Benazzouz | Neuronal Cell Biology | Best Researcher Award

Published on by Cell Biologist

Prof. Abdelhamid Benazzouz | Neuronal Cell Biology | Best Researcher Award

Bordeaux University / Neurodegenerative Diseases Institute | France

Dr. Abdelhamid Benazzouz is a distinguished neuroscientist whose pioneering research has significantly advanced understanding and treatment of Parkinson’s disease. His groundbreaking work during his Ph.D. led to the development of deep brain stimulation (DBS) of the subthalamic nucleus as a novel therapeutic approach for Parkinson’s disease, which was later translated into clinical application. His research focuses on elucidating the mechanisms of action of DBS, exploring the role of monoaminergic systems in the pathophysiology of Parkinson’s disease, and investigating pain mechanisms associated with the disorder. He has led numerous national and international research projects funded by organizations such as the Agence Nationale de la Recherche, Fondation pour la Recherche Médicale, and the Michael J. Fox Foundation. With over 120 publications, more than 24,000 citations, and multiple patents, his contributions span both basic and translational neuroscience. He also leads collaborative research efforts across France, the Netherlands, and Hong Kong to develop innovative therapeutic strategies. As Editor-in-Chief and founder of the Elsevier journal Deep Brain Stimulation, he continues to influence the global neuroscience community, driving forward advancements in neurostimulation, monoaminergic signaling, and the treatment of neurological disorders, particularly Parkinson’s disease and related pain syndromes.

Profiles: Google Scholar | Orcid

Featured Publications:

Krack, P., Batir, A., Van Blercom, N., Chabardes, S., Fraix, V., Ardouin, C., … & Benabid, A. L. (2003). Five-year follow-up of bilateral stimulation of the subthalamic nucleus in advanced Parkinson’s disease. The New England Journal of Medicine, 349(20), 1925–1934.

Limousin, P., Krack, P., Pollak, P., Benazzouz, A. H., Ardouin, C., Hoffmann, D., … & Benabid, A. L. (1998). Electrical stimulation of the subthalamic nucleus in advanced Parkinson’s disease. The New England Journal of Medicine, 339(16), 1105–1111.

Limousin, P., Pollak, P., Benazzouz, A., Hoffmann, D., Le Bas, J. F., Perret, J. E., … & Benabid, A. L. (1995). Effect on parkinsonian signs and symptoms of bilateral subthalamic nucleus stimulation. The Lancet, 345(8942), 91–95.

Benabid, A. L., Pollak, P., Gao, D., Hoffmann, D., Limousin, P., Gay, E., Payen, I., & Benazzouz, A. (1996). Chronic electrical stimulation of the ventralis intermedius nucleus of the thalamus as a treatment of movement disorders. Journal of Neurosurgery, 84(2), 203–214. Benazzouz, A., Gross, C., Féger, J., Boraud, T., & Bioulac, B. (1993). Reversal of rigidity and improvement in motor performance by subthalamic high-frequency stimulation in MPTP-treated monkeys. European Journal of Neuroscience, 5(4), 382–389.

Krack, P., Pollak, P., Limousin, P., Hoffmann, D., Xie, J., Benazzouz, A., … & Benabid, A. L. (1998). Subthalamic nucleus or internal pallidal stimulation in young-onset Parkinson’s disease. Brain: A Journal of Neurology, 121(3), 451–457.

Benabid, A. L., Pollak, P., Gross, C., Hoffmann, D., Benazzouz, A., Gao, D. M., … & Perret, J. (1994). Acute and long-term effects of subthalamic nucleus stimulation in Parkinson’s disease. Stereotactic and Functional Neurosurgery, 62(1–4), 76–84.

Weiping Qin | Spinal Cord Injury | Best Researcher Award

Published on by Cell Biologist

Prof. Dr. Weiping Qin | Spinal Cord Injury | Best Researcher Award

The Icahn School of Medicine at Mount Sinai/James J. Peters VAMC | United States

Dr. Weiping Qin’s research focuses on developing innovative therapeutic strategies to prevent and reverse skeletal and neurological impairments associated with spinal cord injury (SCI). His laboratory investigates the molecular and cellular mechanisms underlying bone loss, muscle atrophy, and neurodegeneration following SCI, with the goal of identifying novel molecular targets for treatment. Dr. Qin’s work integrates approaches from molecular biology, neuroscience, and regenerative medicine to elucidate how injury-induced changes in signaling pathways, inflammation, and oxidative stress contribute to tissue degeneration. He also explores pharmacological and biological interventions that may enhance neural repair, bone regeneration, and functional recovery. Through translational studies, his team aims to bridge fundamental discoveries with clinical applications, advancing potential therapies to improve quality of life and outcomes for patients with SCI. His research has been recognized for its contributions to understanding neurodegenerative and skeletal pathology, and for identifying key therapeutic avenues to promote tissue protection and regeneration.

Profiles:  Google Scholar | Scopus

Featured Publications:

Qin, W., Ho, L., Pompl, P. N., Xiang, Z., Wang, J., Zhao, Z., Peng, Y., Cambareri, G., & others. (2004). Diet-induced insulin resistance promotes amyloidosis in a transgenic mouse model of Alzheimer’s disease. The FASEB Journal, 18(7), 902–904.

Qin, W., Yang, T., Ho, L., Zhao, Z., Wang, J., Chen, L., Zhao, W., Thiyagarajan, M., & others. (2006). Neuronal SIRT1 activation as a novel mechanism underlying the prevention of Alzheimer disease amyloid neuropathology by calorie restriction. Journal of Biological Chemistry, 281(31), 21745–21754.

Qin, W., Haroutunian, V., Katsel, P., Cardozo, C. P., Ho, L., Buxbaum, J. D., & others. (2009). PGC-1α expression decreases in the Alzheimer disease brain as a function of dementia. Archives of Neurology, 66(3), 352–361.

Wang, J., Ho, L., Qin, W., Rocher, A. B., Seror, I., Humala, N., Maniar, K., Dolios, G., & others. (2005). Caloric restriction attenuates β-amyloid neuropathology in a mouse model of Alzheimer’s disease. The FASEB Journal, 19(6), 1–18.

Yamashita, T., Kaneko, S., Shirota, Y., Qin, W., Nomura, T., Kobayashi, K., & others. (1998). RNA-dependent RNA polymerase activity of the soluble recombinant hepatitis C virus NS5B protein truncated at the C-terminal region. Journal of Biological Chemistry, 273(25), 15479–15486.

Shirota, Y., Luo, H., Qin, W., Kaneko, S., Yamashita, T., Kobayashi, K., & others. (2002). Hepatitis C virus (HCV) NS5A binds RNA-dependent RNA polymerase (RdRP) NS5B and modulates RNA-dependent RNA polymerase activity. Journal of Biological Chemistry, 277(13), 11149–11155.