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Mir Ahamed Hossain, Ph.D.

Photo of Dr. Mir Ahamed Hossain, Ph.D.

Research Program Director

Associate Professor of Neurology


Dr. Hossain is an accomplished molecular and 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. more


  • Research Program Director
  • Associate Professor of Neurology

Departments / Divisions



  • Ph.D., University of Calcutta (India) (1990)

Research & Publications

Research Summary

Dr. Hossain’s research experience and background connect basic laboratory research at the levels of cellular/molecular neuroscience and medicine and is 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. One of the laboratory’s ongoing projects is exploring 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.

Another of Dr. Hossain’s lab projects is 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. Yet another project is looking at the molecular bases of neuropathology and neurochemical abnormalities associated with Rett syndrome, and the treatment of osteoporosis using the 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.

Selected Publications

  1. Sex differences in mitochondrial biogenesis determine neuronal death and survival in response to oxygen glucose deprivation and reoxygenation. Sharma J, Johnston MV, Hossain MA. BMC Neurosci. 2014 Jan 10;15:9. doi: 10.1186/1471-2202-15-9. PMID: 24410996
  2. Genetic deletion of NP1 prevents hypoxic-ischemic neuronal death via reducing AMPA receptor synaptic localization in hippocampal neurons. Al Rahim M, Hossain MA. J Am Heart Assoc. 2013 Feb 22;2(1):e006098. doi: 10.1161/JAHA.112.006098. PMID: 23525449
  3. Critical role of neuronal pentraxin 1 in mitochondria-mediated hypoxic-ischemic neuronal injury. Al Rahim M, Thatipamula S, Hossain MA. Neurobiol Dis. 2013 Feb;50:59-68. doi: 10.1016/j.nbd.2012.10.003. Epub 2012 Oct 12. PMID: 23069675
  4. Sex-specific activation of cell death signalling pathways in cerebellar granule neurons exposed to oxygen glucose deprivation followed by reoxygenation. Sharma J, Nelluru G, Wilson MA, Johnston MV, Hossain MA. ASN Neuro. 2011 Apr 7;3(2). pii: e00056. doi: 10.1042/AN20100032. PMID: 21382016
  5. Neuronal pentraxin 1 induction in hypoxic-ischemic neuronal death is regulated via a glycogen synthase kinase-3α/β dependent mechanism. Russell JC, Kishimoto K, O'Driscoll C, Hossain MA. Cell Signal. 2011 Apr;23(4):673-82. doi: 10.1016/j.cellsig.2010.11.021. Epub 2010 Dec 3. PMID: 21130869
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