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Clemens R. Scherzer, M.D.
Phone: 617-768-8427 |
 Brigham and Women's Hospital  Harvard Medical School |
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Clemens R. Scherzer, M.D. is an Associate Neurologist at Brigham and Women’s Hospital, Harvard Medical School, and directs the Laboratory for Neurogenomics at the Center for Neurologic Diseases. He is the Coordinating Principal Investigator of the Edmond J. Safra Global Genetics Consortium on Gene Expression in Parkinson’s disease at the Center for Neurologic Diseases, a Beeson Scholar, and George C. Cotzias Fellow of the American Parkinson’s Disease Association. In his clinical practice he is a movement disorders specialist at Brigham and Women’s Hospital and Massachusetts General Hospital, and directs a biomarker study sponsored by the Michael J. Fox Foundation. He is a graduate of the University of Vienna Medical School, completed internship and neurology residency at Emory University, and fellowship training in movement disorders and in genomics at Massachusetts General Hospital and Harvard Medical School. |
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Our Research The Scherzer Laboratory aims to find disease genes and identify biomarkers for Parkinson’s disease (PD) and other devastating neurodegenerative disorders. We approach our goals with a systematic genome-wide strategy. Instead of testing one gene at a time, we use gene chips to interrogate in parallel expression levels of thousands of genes comprising the entire genome in tissues from patients with PD and other neurodegenerative diseases in order to identify biomarker and susceptibility gene candidates. Candidate genes are tested in human tissues and fly models. Resulting articles have been published in the journals Proceedings of the National Academy of Sciences U. S. A (Scherzer et al 2007), Human Molecular Genetics, Archives of Neurology, Neurobiology of Disease, and Trends in Genetics. Our research is guided by the hypothesis that genome-wide transcript analysis can define biomarkers, susceptibility and modifier genes for complex neurodegenerative diseases by detecting allele-specific gene expression and differential transcription in response to disease proteins. Currently, neurologists can confidently make a diagnosis of PD only when a full-blown clinical picture is present. By that time, 70 percent of dopamine neurons have already died. Earlier detection may make it possible to save much of this vital brain tissue. Simple blood biomarkers for Parkinson’s disease and other neurodegenerative diseases are critically needed for early diagnosis of high-risk individuals and for monitoring disease progression. The lack of blood tests that serve as surrogates of treatment response curtails the development of medications that slow or halt the progression of Parkinson’s disease. We are conducting large clinical biomarker trials to overcome these obstacles and have established the Harvard PD Biomarker Study, a unique longitudinal collection of blood specimens and detailed linked coded clinical data. To identify disease genes we use genome-wide expression scans and genetic validation studies. One of the early successes of this approach was the discovery of a novel disease-modifying gene for Alzheimer’s disease. In a micorarray screen we found with colleagues at Emory that levels of the neuronal sorting receptor SORL1 (also called LR11 or SorLa) are abnormally low in Alzheimer’s patients and for the first time implicated this gene in the disease process (Scherzer et al, 2004). This finding started a new field of investigation with independent groups showing that SORL1 modulates APP trafficking and processing into the amyloid-beta peptide, the principal component of senile plaques in Alzheimer's disease (Andersen et al., 2005; Offe et al., 2006; and others). Further linking SORL1 to Alzheimer's disease, Rogaeva et al. recently found that genetic polymorphisms in this gene are associated with increased susceptibility to the disease. Genomic and genetic analyses of human PD tissues and PD models (Scherzer et al., 2003; Hauser et al., 2005), as well as other neurodegenerative diseases (Li et al., 2003; Xu et al., 2006) have also been performed or are in progress. As part of this effort we have established the international Edmond J. Saffra Global Genetics Consortium: Gene Expression in PD sponsored by the Michael J. Fox Foundation. Together with our collaborators we have already assayed >5 million data points through >200 microarrays in PD patients and in PD models. Data sets include substantia nigra and blood, and a-synuclein-transgenic models in cells, yeast, flies, and mice. |
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