Michael Schlossmacher
mschlossmacher@ohri.ca
Telephone: (613) 562-5800 x8123
Scientist, Neuroscience, Ottawa Hospital Research Institute
Attending Neurologist, Division of Neurology, The Ottawa Hospital
Associate Professor of Medicine (Neurology), cross-appointed to the Department of Cellular & Molecular Medicine, University of Ottawa
Canada Research Chair in Parkinson Disease (tier II), University of Ottawa
Director, MD/PhD Program, Faculty of Medicine, University of Ottawa
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 subsequently 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 Brigham & Women's Hospital (BWH) and Massachusetts General Hospital (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, where he opened a new laboratory in January 2007.
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:
Schlossmacher MG and Mollenhauer B. Biomarker research in Parkinson’s: Objective measures needed for patient stratification in future cause-directed trials. Biom Med 2010;4:1-4
Mollenhauer et al. Cerebrospinal fluid values for alpha-synuclein and tau in patients presenting with parkinsonism. Lancet Neurol 2011;10:230-40
Two, to contribute to the understanding of the cause(s) of PD.
Recent publications on this topic:
Klein et al. Progress in translational neurology and neuroscience 2011: Movement disorders. Arch Neurol 2011; published online February 14th 2011; in press
Hakimi et al. Parkinson’s disease-linked LRRK2 is expressed in circulating and tissue immune cells and upregulated following exposure to microbial structures. J Neural Transm 2011; accepted Apr 21st, 2011; published online May 10th 2011; in press
Three, to explore targets for future cause-directed treatment of PD.
Recent publications on this topic:
Cullen et al., Cathepsin D expression affects the processing, aggregation and toxicity of alpha-synuclein in vivo. Molecular Brain 2009;2:5-11
Cullen et al. Mutations in the acid beta-glucosidase gene linked to Gaucher disease, Parkinson’s and Lewy body dementia dysregulate alpha-synuclein. Ann Neurol 2011; published online March 4th, 2011; in press.
