About Clemens Scherzer, MD

Dr. Scherzer is an Associate Professor of Neurology at Harvard Medical School and directs the Laboratory for Neurogenomics. He is the Coordinating Principal Investigator of the Global Parkinson's Disease Gene Expression Consortium (GPEX). He received the Paul B. Bees on Awar d of the American Federation for Aging Research and the National Institute on Aging, and a Dr. George Cotzias Memorial Award of the American Parkinson's Disease Association. He completed neurology residency at Emory University and fellowship training in movement disorders and in genomics at Massachusetts General Hospital and Harvard Medical School. In his clinical practice he works as a movement disorders specialist at Brigham and Women's Hospital and Massachusetts General Hospital, and is the Co-Director of the Harvard NeuroDiscovery Biomarker Study.

Clinical Interests:




Mass General Neurology
55 Fruit St.
Boston, MA 02114
Phone: 855-644-6387

McLean Hospital
115 Mill St.
Belmont, MA 02478
Phone: 617-855-3141

Medical Education

  • MD, University of Vienna
  • Residency, Emory University School of Medicine
  • Fellowship, Brigham and Women's/Massachusetts General Hospital

American Board Certifications

  • Neurology, American Board of Psychiatry and Neurology

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We apply genomic approaches to the detection, characterization, and treatment of Parkinson's disease (PD). Our leading hypothesis is that genome-wide expression analysis can define biomarkers, modifier and susceptibility genes for complex neurodegenerative diseases by detecting allele-specific gene expression and differential transcription in response to disease proteins. We identify and test candidate genes in clinical studies and cellular and animal models.

In Alzheimer's disease (AD), our original discovery of abnormally low message levels of the neuronal sorting receptor SORL1/LR11 in patients with AD (Scherzer et al., Archives of Neurology, 2004) started a new field of investigation. SORL1/LR11 directs Amyloid0?? trafficking and is now linked to genetic susceptibility for AD.

Leads are discovered and developed into clinically useful blood tests for diagnosing, predicting and tracking disease progression in our several large, well-designed clinical biomarker studies. These includes the unique, two-year, longitudinal, Harvard NeuroDiscovery Biomarker Study of 2,000 patients and controls.

The laboratory is funded by the National Institute of Neurological Disorders and Stroke, the National Institute on Aging, the Michael J. Fox Foundation, the American Federation for Aging Research, and the Harvard NeuroDiscovery Center.


  • Zheng B, Liao Z, Locascio JJ, Lesniak KA, Roderick SS, Watt ML, Eklund AC, Zhang-James Y, Kim PD, Hauser MA, Gr??nblatt E, Moran LB, Mandel SA, Riederer P, Miller RM, Federoff HJ, W??llner U, Papapetropoulos S, Youdim MB, Cantuti-Castelvetri I, Young AB, Vance JM, Davis RL, Hedreen JC, Adler CH, Beach TG, Graeber MB, Middleton FA, Rochet JC, Scherzer CR; Global PD Gene Expression (GPEX) Consortium. PGC-4??, a potential therapeutic target for early intervention in Parkinson's disease. Sciend Translational Medicine, 2010 Oct 6;2(52):52ra73. PubMed | Reprint

    Lipinski MM, Zheng B, Lu T, Yan Z, Py BF, Ng A, Xavier RJ, Li C, Yankner BA, Scherzer CR, Yuan J. Genome-wide analysis reveals mechanisms modulating autophagy in normal brain aging and in Alzheimers disease. Proceedings of the National Academy of Sciences U.S.A, 107(32): 14164-9, 2010 PubMed

    Khurana V, Elson-Schwab I, Fulga TA, Sharp KA, Loewen CA, Mulkearns E, Tyynel?? J, Scherzer CR, Feany MB. Lysosomal dysfunction promotes cleavage and neurotoxicity of tau in vivo. PLoS Genet. 2010 Jul 15;6(7):e1001026. PubMed

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