Ellen
Hess, Ph.D.
Our investigations
focus on determining the molecular genetic basis of inherited neurologic
disorders, particularly movement disorders. We are currently interested
in the molecular mechanisms regulating two classes of movement disorders
including dystonia and hyperactivity disorders such as ADHD and Tourette
syndrome. We use neurological mouse mutants, transgenics and knockout,s
to model brain dysfunction on the molecular, cellular and behavioral levels.
Incorporating classical neuroscience techniques, including pharmacology,
behavior and anatomy, with genetics and molecular biology provides a global
approach to unraveling these disorders. For example, we have identified
a gene that causes hyperactivity in mice and have rescued the hyperactivity
using a transgenic gene replacement strategy; we are currently using behavioral
and cellular pharmacology to understand the cellular mechanisms that give
rise to the hyperactivity. Ultimately, the goal is to develop novel therapeutics
using the mouse models as guides.
CURRENT
ADDRESS
The
Johns Hopkins Hospital
Department of Neurology
Meyer 6-181
600 N. Wolfe Street
Baltimore, MD 21287
Phone: 410-502-7511
Fax: 410-502-6737
E-Mail: ehess@jhmi.edu
EDUCATION
& TRAINING
- 1983
B.A., Psychobiology, magna
cum laude with honors
Wellesley College, Wellesley, MA
- 1987
Ph.D., Neuroscience, University of California, San Diego
San Diego, CA
CURRENT
APPOINTMENTS
- Associate
Professor of Neurology
The Johns Hopkins University School of Medicine
- Associate
Professor of Neuroscience
The Johns Hopkins University School of Medicine
HONORS
& AWARDS
- 1982,
Phi Beta Kappa
- 1983-84,
Regents Scholarship, University of California
- 1985-87,
PHS NIMH Predoctoral Fellowship, MH09535
- 1990-92,
American Epilepsy Society Research Fellowship
- 1994-97,
Klingenstein Fellow
- 1997-99,
NARSAD Young Investigator
- 1997,
Tourette Syndrome Association Award
- 1997,
Pennsylvania State University Hinkle Society Young Investigator Award
RESEARCH
ACTIVITIES
- Molecular
genetic regulation of behavior with emphasis on abnormal behavior and
movement disorders
- Mutant
and Transgenic mouse models of neurological disease
- Calcium
channel expression and function
- Monoamine
neurochemistry
- regulation
of neurotransmitter release
REPRESENTATIVE
PUBLICATIONS
- Hess,
E.J. Migraines in Mice? Cell, 87:1149-1151, 1996.
- Campbell,
D.B. and Hess, E.J. Cerebellar circuitry is activated during
convulsive episodes in the tottering (tg/tg) mutant mouse. Neuroscience,
85:773-783, 1998.
-
Campbell, D.B. and Hess, E.J. L-type calcium channels contribute
to the tottering mouse dystonic episodes. Molecular Pharmacology, 55:23-31,
1999.
-
Campbell, D.B., North, J.B. and Hess, E.J. Tottering mouse motor
dysfunction is abolished on the Purkinje cell degeneration (pcd) mutant
background. Experimental Neurology, 160:268-278, 1999.
- Jinnah,
H.A., Sepkuty, J.P., Ho, T., Drew, T., Rothstein, J.D. and Hess,
E.J. Calcium channel activation and dystonia in the mouse. Movement
Disorders, 15:542-551, 2000.
-
Jones,
M.D., Williams, M.E. and Hess, E.J. Abnormal presynaptic catecholamine
regulation in a SNAP-25 deficient hyperactive mouse mutant. Pharmacology
Biochemistry & Behavior, 68:669-676, 2001
- Fureman, B.E., Jinnah, H.A. and Hess, E.J. Paroxysmal dyskinesia
in the calcium channel mouse mutant tottering, Pharmacology Biochemistry
& Behavior, 73:631-637, 2002.
- Pizoli, C.E. Jinnah, H.A., Billingsley, M.L. and Hess, E.J.
Abnormal cerebellar signaling induces dystonia in mice, Journal of Neuroscience,
22:7825-7833, 2002.
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