Overview
Steven W. Levison graduated from the University of Rochester, where he received a B.S. in
Neuroscience in 1983. He completed a Ph.D. in Neurobiology in 1990 at UNC-Chapel Hill, followed by a
postdoctoral fellowship in the Program in Neurobiology and Behavior at Columbia University. Dr. Levison
joined the faculty of New Jersey Medical School in 2004 after 11 years on the faculty of the Penn State
College of Medicine. He presently holds the position of Professor in the Department of Pharmacology,
Physiology and Neuroscience and Directs the Laboratory for Regenerative Neurobiology. Dr. Levison has
authored over 100 peer-reviewed scientific articles and his research has been supported for over 30 years by
the NIH and state and non-profit foundations. He is recognized internationally for his pioneering studies that
have established that there is a regenerative response from the endogenous neural stem cells of the
subventricular zone. Ongoing studies are deciphering how brain development is affected by infections during
pregnancy contributing to neurological and psychiatric disorders. Other studies are manipulating those signals
that regulate neurogenesis, gliogenesis and neuronal survival towards the goal of producing new therapies to
both protect the immature brain from tertiary injuries sustained by hypoxic-ischemic and traumatic brain
injuries and enhance cell replacement and regeneration.
Education
B.S., 1983, University of Rochester, Neuroscience, NY, Neuroscience
PHD, 1990, University of North Carolina at Chapel Hill, NC, Neurobiology
Curriculum Vitae
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Director, Laboratory for Regenerative Neurobiology
Ongoing studies in Dr. Levison?s laboratory center on establishing which cytokines and growth factors
participate in the self-renewal of the neural stem cells in the brain, how the stem cells and progenitors respond
to environmental signals and brain damaging events and how to protect the brain from tertiary injury after
stroke and traumatic brain injuries.
There are currently 3 major ongoing research projects in the lab. One project seeks to characterize
progenitors that reside within the subventricular zone. These studies will: 1) Establish when specific
multipotential and bipotential progenitors emerge during mouse development; 2) Define the transcripts
expressed by individual progenitors using bulk and single cell RNAseq. 3) Define changes in gene transcription
that correspond with developmental restriction and specification; and 4) Establish which types of neurons and
glia are produced from each progenitor subtype. These formative studies will lay the foundation for a decade
of future work to understand how these progenitors participate in neural development across species, how
they are affected by environmental stimuli that disturb normal brain development leading to brain disorders
and how these progenitors might be recruited to participate in regeneration and repair of the nervous system
after injury.
The second major project in the lab is exploring how immune system activation modifies neural development
towards the goal of understanding how maternal infections contribute to autism spectrum disorder (ASD)
incidence. Our published data support the hypothesis that elevated levels of IL-6 in the immature brain alters
the output of the secondary neuroepithelial cells of the subventricular zone and the subgranular zone. To test
this hypothesis, we have performed in vitro studies to determine how IL-6 affects the growth of these
secondary neuroepithelial cells. Then, to establish how elevated levels of IL-6 affect the neural development,
we have produced a new model of ASD where we inject postnatal day 3-6 mouse pups with IL-6. Ongoing
studies are exploring whether neurogenesis or gliogenesis are altered. In addition, the mice are being
subjected to a battery of behavioral tasks to assess learning, memory, anxiety and social interactions. The
data obtained from these studies will lend additional support for the therapeutic neutralization of IL-6 in
premature and neonatal infants at risk for developing ASD.
The third major project in the lab is exploring the regenerative and neuroprotective properties of the
cytokine leukemia inhibitory factor (LIF) in recovery from perinatal hypoxia-ischemia and from concussive head
injuries. Our studies are: 1) testing the hypothesis that LIF haplodeficient mice will sustain greater
neuronal and glial cell damage after injury accompanied by worse neurological disabilities; 2) test the
hypothesis that the extent of injury can be reduced and that the natural expansion of resident neural
progenitors can be amplified by intranasal LIF administration and 3) to determine the mechanisms through
which LIF is producing its neurotrophic actions. Completing these experiments will provide key insights into
neurodegenerative processes after brain injury as well as reveal whether a single cytokine can both protect the
brain from injury and amplify the neuroregenerative responses of the resident neural progenitors to
improve function
