Mir Ahamed Hossain, Ph.D.

Dr. Mir Ahamed Hossain
Mir Ahamed Hossain
Research Program Director, Training Administration Research Program (TARP)

Kennedy Krieger Institute
707 N. Broadway
Baltimore, MD 21205
Phone: (443) 923-2678
Email: hossain@kennedykrieger.org

Dr. Mir Ahamed Hossain is a research scientist and research program director for the Training Administration Research Program (TARP) at the Kennedy Krieger Institute. He is an associate professor of neurology at the Johns Hopkins University School of Medicine.

Biographical Sketch:

Dr. Hossain is an accomplished molecular/cellular biologist with considerable expertise in experimental neuroscience and brain injury.  Dr. Hossain is widely recognized for his work in hypoxic-ischemic injury in neonatal brain and understanding the mechanism(s) of neuroprotection and survival. Dr. Hossain pursued his graduate education in Biochemistry with major in Neuroscience at the University of Calcutta, India, where he obtained his Ph.D. in Biochemistry.  He came to the United States for postdoctoral fellowships first in the Department of Pharmacology at the University of Colorado, and then in the Department of Neuroscience at the Johns Hopkins University School of Medicine and Department of Neurology at Kennedy Krieger Institute. In 1997, he joined the Kennedy Krieger Institute as a faculty member. He is also a research program director for the Training Administration Research Program (TARP) at the Kennedy Krieger Institute.

Dr. Hossain is a member of the American Society for Pharmacology and Experimental Therapeutics, the Society for Neuroscience, American Society for Neurochemistry and American Heart Association. He was awarded the Junior Research Fellow Scholarship by the Indian Government’s Indian Council of Medical Research, and Scientist Development award from the national center of the American Heart Association.

Research Summary:

Dr. Hossain’s research experience and background interface between the basic laboratory research at the levels of cellular/molecular neuroscience and medicine; directed towards understanding the fundamental causes of neonatal brain injury, neurodevelopmental disabilities and human neurodegenerative diseases.  Cerebral hypoxia-ischemia (HI) during the critical perinatal/neonatal stages is the single most important cause of acute mortality and chronic neurological disabilities in surviving infants and children. Despite advances in the prognoses and management of brain injury, specific therapy remains elusive.  

The major focus of Dr. Hossain's laboratory (Cellular and Molecular Neurology Laboratory) has been on hypoxic-ischemic injury in developing brain to identify novel molecular and cellular factors contributing to neuronal death, neurodegeneration, and understanding the mechanisms of neuroprotection and endogenous neurogenesis within the brain. In one of the ongoing projects, Dr. Hossain’s laboratory is investigating the role of a novel neuronal family of proteins involved in neonatal hypoxic-ischemic brain injury, cellular and molecular determinants of the cell death and survival pathways and sexual dimorphism in neuronal death pathways. On a different project, Dr. Hossain’s lab is also investigating the effects of chronic hyperglycemia on pancreatic β-cells and toxic effects of glucose “glucotoxicity” in the brain, which might share a common mechanism involving novel molecular target(s)-dependent development of diabetes, hyperglycemia-induced neurotoxicity and neurological deficits. On a third project, his lab is investigating the molecular basis of neuropathology and neurochemical abnormalities associated with the neurodevelopmental disorder ‘Rett Syndrome’, and the treatment of osteoporosis using murine Rett Syndrome model.

Dr. Hossain’s investigations concentrate on the preclinical model systems of both in vivo neonatal animal model of hypoxia-ischemia and in vitro primary neuronal cell cultures, involving both cell biology and molecular biological techniques. His laboratory is the first to identify a novel neuronal protein "neuronal pentraxin 1" contributing to hypoxia-ischemia induced neuronal injury in neonatal brain. His research on lead neurotoxicity is the first demonstration of lead-induced gene expression of a growth factor, and the first detailed dissection of the second messenger pathways and transcription factors that mediate the effects of lead on gene expression in CNS cells. Dr. Hossain's lab also provides first evidence for enhanced neuronal injury/death and the role of MeCP2 in excitotoxicity using primary cerebellar granule neurons as an in vitro Rett syndrome model. His goals are to understand the fundamental causes of brain injury and human neurodegenerative diseases and their potential prevention. Dr. Hossain's research will help to identify novel molecular targets within the central neurons that could become the basis for developing broadly applicable neuroprotective strategies for the treatment of neonatal brain injury with the aim to improve post-injury cerebral functions and recovery. 

LINK: SciVal Experts Research Profile for Mir Ahamed Hossain

Research Publications: 

Al Rahim M., Thatipamula S. and Hossain M.A.. (2013). Critical role of neuronal pentraxin 1 in mitochondria-mediated hypoxic-ischemic neuronal injury. Neurobiology of Disease, 50, 59-68.

Hossain M.A.. (2012). Genetic deletion of NP1 prevents hypoxic-ischemic neuronal death via reducing AMPA receptor synaptic localization in hippocampal neurons. Journal of the American Heart Association. doi:10.1161/JAHA.112.000050.

Al Rahim M., Thatipamula S. and Hossain M.A.. (2013). Molecular determinants of Hypoxic-ischemic injury in developing brain and potential strategies for neuroprotection (Book Chapter), In Brain Damage: Causes, management and Prognosis. Editors: Aleric J. Schäfer and Johann Müller. Nova Science Publishers, Hauppauge, NY, pp. 71-100.

Sharma, J., Nelluru, G., Wilson, M.A., Johnston, M.V. and Hossain M.A.. (2011). Sex-specific activation of cell death signaling pathways in cerebellar granule neurons exposed to oxygen glucose deprivation followed by reoxygenation. ASN Neuro, 3(2), 85-97.

Russell, J. C., Kishimoto K., O'Driscoll C. and Hossain M.A.. (2011). Neuronal pentraxin 1 induction in hypoxic-ischemic neuronal death is regulated via a glycogen synthase kinase-3α/β dependent mechanism. Cellular Signaling, 23(4), 673-682.

Hossain M.A.. (2008). Hypoxic-ischemic injury in neonatal brain: involvement of a novel neuronal molecule in neuronal cell death and potential target for neuroprotection. International Journal of Developmental Neuroscience, 26(1), 93-101.

Russell, J. C., Whiting H., Szuflita N. and Hossain M.A.. (2013). Nuclear translocation of X-linked inhibitor of apoptosis (XIAP) determines cell fate after hypoxia ischemia in neonatal brain. Journal of Neurochemistry, 106(3), 1357-1370.

Russell, J. C., Szuflita N., Khatri R., Laterra J. and Hossain M.A.. (2006). Transgenic expression of human FGF-1 protects against hypoxic-ischemic injury in perinatal brain by intervening at caspase-XIAP signaling cascades.. Neurobiology of Disease, 22(3), 677-690.

Hossain M.A.. (2005). Molecular mediators of hypoxic-ischemic injury and implications for epilepsy in the developing brain.. Epilepsy & Behavior, 7(2), 204-213.

Hossain M.A., Russell J. C., O'Brien R. and Laterra J. (2004). Neuronal pentraxin 1: a novel mediator of hypoxic-ischemic injury in neonatal brain.. The Journal of Neuroscience, 24(17), 4187-4196.

Luo H. R., Hattori H., Hossain M. A., Hester L., Huang Y., Lee-Kwon W., et al. (2003). Akt as a mediator of cell death. Proceedings of the National Academy of Sciences of the United States of America, 100(20), 11712-11717.

Walter K. A., Hossain M. A., Luddy C., Goel N., Reznik T. E. and Laterra J. (2002). Scatter factor/hepatocyte growth factor stimulation of glioblastoma cell cycle progression through G(1) is c-Myc dependent and independent of p27 suppression, Cdk2 activation, or E2F1-dependent transcription. Molecular and Cellular Biology, 22(8), 2703-2715.

Hossain, M. A., Russell J. C., Gomez R., Laterra J., & Gomes R. (2002). Neuroprotection by scatter factor/hepatocyte growth factor and FGF-1 in cerebellar granule neurons is phosphatidylinositol 3-kinase/akt-dependent and MAPK/CREB-independent. Journal of Neurochemistry, 81(2), 365-378.