02/09/2010 














Michael Schlossmacher,
mschlossmacher@ohri.ca
Telephone: (613) 562-5800 x8123

Roger Guindon Hall (see Contact page for maps)




Scientist, Neuroscience, Ottawa Hospital Research Institute

Canada Research Chair in Parkinson Disease (tier II)

Associate Professor of Medicine (Neurology), cross-appointed to the Department of Cellular and Molecular Medicine, University of Ottawa

Attending Neurologist, Division of Neurology, The Ottawa Hospital

Biographical Sketch

The goal of Dr. Schlossmacher's work as a physician-scientist is to contribute to the improved care of patients with neurodegenerative diseases. In 1988, following his graduation from medical school in Vienna, Austria and the completion of his military service, a Fulbright Commission scholarship enabled Dr. Schlossmacher to visit Harvard University. In the laboratory of Dr. Dennis Selkoe (1988-1992), he studied the molecular pathology of Alzheimer disease. Following residency training in general medicine from 1992 to 1995 in Vienna, Austria, Dr. Schlossmacher completed adult neurology training in the Harvard Longwood Neurology Program (1995-1999) and a clinical fellowship in the subspecialty of movement disorders at Massachusetts General Hospital and Brigham & Women's Hospital (BWH; 1999-2001). Since 2000, Dr. Schlossmacher has focused his research activities on Parkinson disease, first, under the mentorship of Drs. Dennis Selkoe, Ken Kosik and Peter Lansbury, and then, as of 2003, as an independent investigator at the Center for Neurologic Diseases at BWH in Boston. In January 2004, he was appointed Assistant Professor in Neurology at Harvard Medical School. In late 2006, Dr. Schlossmacher moved to the University of Ottawa.

Research

The Schlossmacher laboratory is pursuing three complementary goals:

One, to contribute to the development of a biomarker for Parkinson disease (PD).
Recent publications on this topic:
Klein C and Schlossmacher MG. The genetics of Parkinson disease: Implications for neurological care. Nat Clin Pract Neurol 2006;2:136-46
Mollenhauer B et al. Direct quantification of CSF -synuclein by ELISA and first cross-sectional study of patients with neurodegeneration. Exper Neurol 2008;213(2):315-25.

Two, to contribute to the understanding of the cause(s) of PD.
Recent publications on this topic:
Klein C and Schlossmacher MG. Parkinson disease, 10 years after its genetic revolution: Multiple clues to a complex puzzle. Neurology 2007;69:2093-2104
LaVoie MJ et al. The effects of oxidative stress on Parkin and other E3 ligases. J Neurochem 2007;103:2354-2368

Three, to explore targets for cause-directed treatment of PD.
Recent publications on this topic:
Scherzer CR et al. GATA transcription factors directly regulate the Parkinson's disease-linked gene -synuclein. PNAS USA 2008;105(31):10907-12
Cullen V et al. Cathepsin D expression affects the processing, aggregation and toxicity of -synuclein in vivo. Mol Brain 2009; in press


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