Steven W. Levison

Dr. Steven W. Levison

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Research Focus & Metrics

Academic Career Length

38Years (1989-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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17 February 2015 in Nature Reviews Neurology
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HHHenrik Hagberg
Henrik Hagberg
CMCarina Mallard
Carina Mallard
DFDonna M. Ferriero
Donna M. Ferriero
SVSusan J. Vannucci
Susan J. Vannucci
SLSteven W. Levison
Steven W. Levison
PGPierre Gressens
Pierre Gressens

1 February 1993 in Neuron
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Journal Article
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SLSteven W. Levison
Steven W. Levison
JGJames E. Goldman
James E. Goldman

1 May 2005 in Diabetes
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Journal Article
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JKJ. Kyle Krady
J. Kyle Krady
ABAnirban Basu
Anirban Basu
CAColleen M. Allen
Colleen M. Allen
YXYuping Xu
Yuping Xu
KLKathryn F. LaNoue
Kathryn F. LaNoue
SLSteven W. Levison
Steven W. Levison
Diabetes leads to vascular leakage, glial dysfunction, and neuronal apoptosis within the retina. The goal of the studies reported here was to determine the role that retinal microglial cells play in diabetic retinopathy and assess whether minocycline can decrease microglial activation and alleviate retinal complications. Immunohistochemical analyses showed that retinal microglia are activated early in diabetes. Furthermore, mRNAs for interleukin-1β and tumor necrosis factor-α, proinflammatory mediators known to be released from microglia, are also increased in the retina early in the course of diabetes. Using an in vitro bioassay, we demonstrated that cytokine-activated microglia release cytotoxins that kill retinal neurons. Furthermore, we showed that neuronal apoptosis is increased in the diabetic retina, as measured by caspase-3 activity. Minocycline represses diabetes-induced inflammatory cytokine production, reduces the release of cytotoxins from activated microglia, and significantly reduces measurable caspase-3 activity within the retina. These results indicate that inhibiting microglial activity may be an important strategy in the treatment of diabetic retinopathy and that drugs such as minocycline hold promise in delaying or preventing the loss of vision associated with this disease.

1 December 2002 in Survey of Ophthalmology
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Journal Article
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TGThomas Gardner
Thomas Gardner
DADavid Antonetti
David Antonetti
ABAlistair J. Barber
Alistair J. Barber
KLKathryn F LaNoue
Kathryn F LaNoue
SLSteven W. Levison
Steven W. Levison

1 June 2005 in Investigative Ophthalmology & Visual Science
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Journal Article
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ABAlistair J. Barber
Alistair J. Barber
DADavid Antonetti
David Antonetti
TKTimothy S. Kern
Timothy S. Kern
CRChad E. N. Reiter
Chad E. N. Reiter
RSRohit S. Soans
Rohit S. Soans
SBSarah K. Bronson
Sarah K. Bronson
Purpose. This study tested the Ins2Akita mouse as an animal model of retinal complications in diabetes. The Ins2Akita mutation results in a single amino acid substitution in the insulin 2 gene that causes misfolding of the insulin protein. The mutation arose and is maintained on the C57BL/6J background. Male mice heterozygous for this mutation have progressive loss of β-cell function, decreased pancreatic β-cell density, and significant hyperglycemia, as early as 4 weeks of age.

26 April 2004 in Journal of Neurochemistry
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Journal Article
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CLChristina M. Liberto
Christina M. Liberto
PAP. J. Albrecht
P. J. Albrecht
LHL. M. Herx
L. M. Herx
VYV. W. Yong
V. W. Yong
SLSteven W. Levison
Steven W. Levison