Dr. Venna obtained his Bachelor’s Degree in Pharmacy from Gulbarga University, India. He received his PhD in 2009 from the University of Lille-2, France. Much of his doctoral work focused on behavior and the response to pharmacological agents for the treatment of depression. After completing his Ph.D., Dr. Venna joined Dr. McCullough’s Cerebrovascular Research Group to obtain his post-doctoral training in ischemic stroke research. He was subsequently appointed as faculty at the University of Connecticut Health Center. In 2015, Dr. Venna joined the Department of Neurology at UTHealth in Houston, TX.
Because of his long-standing interest in basic and translational stroke research, Dr. Venna and his research team have established translationally relevant stroke models in rodents. These models mimic the human disease and allow for the investigation and elucidation of the underlying mechanisms that determine acute and long-term outcomes after stroke.
Dr. Venna has published his research findings in several prestigious journals, including Stroke, Neuroscience, Translational Psychiatry, Psychoneuroendocrinology, Acta Neuropathologica and the European Journal of Neuroscience. He received a number of awards and honors, including the American Heart Association Young Investigator Travel Award, Founders Affiliate Grants from AHA and the French Pharmacological Society Fellowship Award. His research is currently supported by Scientist Development Grant from the American Heart Association.
Dr. Venna is currently working on several translational research projects in the field of ischemic stroke. His work primarily focuses on the identification and development of novel therapeutic approaches to improve ischemic stroke outcomes by reducing neuronal death and enhancing post-stroke recovery. In line with his previous behavioral research interests, Dr. Venna utilizes a variety of experimental models to explore the mechanisms underlying post-stroke depression and cognitive impairment.
One of Dr. Venna’s current projects examines the role macrophage migration inhibitory factor (MIF) in post-stroke outcome in young and aged animals. MIF is a cytokine that plays a key role in inflammation and innate immune signaling in both central and peripheral tissue. Importantly, MIF has recently been identified as a major contributor to depression. Although it is well accepted that depression contributes to impaired recovery after stroke, it remains unclear whether MIF signaling contributes to post-stroke depression and recovery. Dr. Venna is currently performing detailed and translationally relevant studies to elucidate the role of MIF signaling on depression and functional recovery after ischemic stroke. This project will help us better understand the underlying mechanisms involved in post-stroke recovery, facilitate the identification of reliable biomarkers of stroke recovery and serve as the basis for the development of future therapeutics for use in stroke patients.