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| Faculty > Jonathan Rosand |
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Jonathan Rosand, M.D.
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Jonathan Rosand,
M.D., MSc.
Associate Professor of Neurology Harvard Medical
School
Director, Division of Neurocritical Care and Emergency
Neurology
Department of Neurology, Mass General Hospital
Director, MGH Neuroscience Intensive Care Unit
Faculty member, Program in Medical and Population
Genetics, Broad Institute
Center for Human Genetic Research Richard B.
Simches Research Center CPZN-6810
185 Cambridge Street
Boston MA 02114 USA
Contact: Katrina Screen
kscreen@partners.org
Phone: (617) 724-2698
Fax: (617) 643-3293
jrosand@partners.org
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Jonathan Rosand is Director of the
Division of Neurocritical Care and Emergency
Neurology, Director of the Neuroscience Intensive
Care Unit, and an independent faculty member
within the Center for Human Genetic Research
at Massachusetts General Hospital. In addition
he is a faculty member within the Program
in Medical and Population Genetics of the
Broad Institute. Prior to becoming the founding
director of the Division of Neurocritical
Care and Emergency Neurology, Dr. Rosand directed
the Massachusetts General Hospital/Brigham
and Women's Hospital/Harvard Medical School
Fellowship Training Program in Vascular and
Critical Care Neurology. This program, the
largest in the United States, trains neurologists
in all aspects of stroke care and critical
care neurology.
The overall goal of our lab is to leverage
the rapid growth in neuroimaging and human
genetics with the goal to reduce the burden
of intracerebral hemorrhage and stroke. There
are three main areas of focus to our work:
Intracerebral hemorrhage
Accounting for between 15% and 25% of strokes,
ICH is fatal in 30% - 60% of individuals and
leaves a substantial proportion of survivors
with permanent disability. ICH is also the
most feared complication of chronic anticoagulation,
and this fear is often a motivation for withholding
anticoagulants from elderly patients. We have
applied epidemiological and imaging analysis
to elucidate the biology of ICH. They have
identified amyloid angiopathy and leukoaraiosis
as risk-factors for ICH in patients on warfarin,
providing strong evidence that it is the presence
of underlying cerebrovascular disease, rather
than exposure to anticoagulation alone, that
causes ICH in this population. Examinations
of the acute clinical course of warfarin-related
ICH have demonstrated that patients taking
warfarin at the time of ICH have twice the
rate of death compared to those patients not
taking warfarin, and that this markedly elevated
mortality appears to be due to higher rates
of hematoma expansion and delayed bleeding.
We have developed the
FUNC score for prediction of functional recovery
from ICH, and are currently investigating
CT angiography for the identification of ongoing
bleeding in patients with ICH.
Leukoaraiosis and ischemic brain injury
Leukoraiosis, also known as white matter disease,
is a common radiographic finding in the aging
population. Easily visualized on CT and MRI
of the brain, its presence is associated with
risk of stroke, cognitive decline, gait disorders,
and late-life depression. Inherited genetic
factors appear to play a substantial role
in determining the severity of leukaraiosis.
In collaboration with investigators from the
Martinos Center for Biomedical Imaging we
have demonstrated that the severity of leukoaraiosis
at the time of acute ischemic stroke influences
the degree to which the brain can withstand
the damage caused by the stroke. We are now
carrying out genome-wide association studies
to identify the genetic determinants of leukoaraiosis,
with the ultimate goal of finding novel biological
targets for improving stroke outcome.
The role of genetic variation in ICH
and stroke
Ongoing studies seek the genetic determinants
of risk of stroke as well as the genetic determinants
of functional recovery from these neurologic
injuries. Because of our location within the
CHGR and Broad Institute community, our group
is able to leverage local strengths in analytical
genetics for the development of cutting-edge
and rigorous approaches to gene discovery.
In addition, we have collaborated with Mark
Eckman at the University of Cincinnati, to
apply decision-analysis to determine whether
genetic testing can improve bedside decision-making
for patients who are candidates for long-term
anticoagulation.
Dr. Rosand has devoted substantial effort
to assembling the tools necessary for state-of-the-art
investigations of common genetic variants
and human disease. Most notable of these
has been the International Stroke Genetics
Consortium (www.strokegenetics.org), which
formed in April, 2007. Members include 30
leading centers in Europe, North America,
Australia and Asia that have committed to
performing adequately powered stroke genetics
studies involving tens of thousands of well-characterized
patients. Successes have included the securing
of substantial grant awards from the Wellcome
Trust, NIH, and Australian National Research
Council for large-scale genome-wide association
studies, as well as the identification of
susceptibility loci for both ischemic stroke
and ICH.
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