DepartmentCellular and Integrative Physiology
Abdulhafiz Danju Imam Aliagan
Jean C. Bopassa, Ph.D
Hobbies and Interests:
Soccer, Badminton and reading
Bachelor's; 2009-2013 Kwara State University, Malete Nigeria (Microbiology)
Masters: 2015-2017 Texas A&M University, Kingsville (Biology)
P.hD.: 2017- till date, University of Texas Health, San Antonio
I am working on elucidating the role of the inner mitochondrial membrane protein (Mic60/Mitofilin) in Parkinson’s disease.Mitochondrial dysfunction is a major hallmark in many diseases including Parkinson’s disease, and Mic60/Mitofilin dysregulation plays a key role in mitochondrial dysfunction. The goal of my research is to understand the mitochondrial-dependent mechanism leading to mitochondrial dysfunction and ultimately dopaminergic neuron death in Parkinson disease, using mouse models and in vitro models. I combine various multidisciplinary approaches including biochemical, molecular biology, genetics, neuroscience and microscopic approaches to elucidate the mechanism of Mic60 downregulation, and how to protect against this downregulation to induce neuroprotection.
Awards & Accomplishments
Invited platform presenter, Perry & Ruby Stevens Parkinson’s Disease Center of Excellence, San Antonio, TX.
Feng, Y., Madungwe, N.B., Imam Aliagan, A.D., Tombo N., and Bopassa, JC (2019). Liproxstatin-1 protects the mouse myocardium against ischemia/reperfusion injury by decreasing VDAC1 levels and restoring GPX4 levels. Biochem Biophys Res Commun. 2019 Oct 14. pii: S0006-291X(19)31897-2. doi: 10.1016/j.bbrc.2019.10.006.
Imam Aliagan A.D, Daraei M.A, Feng, Y., Liu L, Madungwe, N.B., Tombo, N., and Bopassa J.C (2019) Mitofilin
Interacts with Parkin in the Inner Mitochondrial Membrane to Increase Dopaminergic Neuron Death in Response to PD Stressors. In review.
Madungwe, N.B., Feng, Y., Imam Aliagan, A.D., Tombo, N., Kaya, F., and Bopassa, J.C. (2019). Inner
mitochondrial membrane protein MPV17 mutant mice hearts display impaired cardiac functional recovery after ischemia/reperfusion via dysregulation of the mitochondrial permeability transition pore. In review.