Boston University | Alzheimer's Disease Center | Our Team | Faculty

Henry Querfurth, MD, PhD

Associate Professor of Neurology

Phone: 617.789 2685
Fax: 617.789 5177
Email: henry.querfurth@tufts.edu
Location: Caritas St. Elizabeth's Medical Center, Tufts University

Websites: www.caritas-semc.org www.neurosci.tufts.edu

Background

Dr Querfurth completed his MD and PhD training in Neuroscience at the University of Rochester as an MD PhD. He completed two residencies, in Internal Medicine and Neurology, at the University of Washington, Seattle. Dr. Querfurth is board certified in Neurology and Internal Medicine. He obtained post-doctoral training in Neurodegeneration and Dementia at the Center for Neurologic Diseases, Brigham and Women’s Hospital. He is a full-time clinical staff member in the Dept. of Neurology, Caritas St. Elizabeth’s Medical Center and Tufts University where he also serves as director of Neurology Research.

Research Interests

Dr. Querfurth’s interests are focused on basic Alzheimer’s disease mechanisms as well as on the pathophysiology of the biochemically related disorder, Inclusion Body Myositis. He investigates abnormalities in signal pathways and ion homeostasis related to b-amyloid and tau deposition and expression.

ADC Role

At present, Dr. Querfurth serves as clinical consultant to the ADC and is the recipient of an ADC Pilot Award to investigate b APP metabolism in skeletal muscle tissue.

Awards/Memberships

Dr. Querfurth is principal investigator of NIH funded research and member of the Society for Neuroscience.

Recent Publications

Querfurth, H.W., Suhara, T., Rosen, K.M., McPhie, D.L., Fujio, Y., Tahini, G., Neve, R.L., Adelman, L.S., and Walsh, K., 2001, b-amyloid peptide expression is sufficient for myotube death: Implications for human Inclusion Body Myopathy. Mol. Cell. Neurosci., 17:793-810.[PubMed]

Suhara, T., Magrane, J., Rosen, K.M., Walsh, K., and Querfurth, H. 2003, A b42 generation is toxic to endothelial cells and inhibits eNOS function through an Akt/GSK3 b signaling-dependent mechanism. Neurobiology of Aging 24/3 437-451. [PubMed]

Rosen, K., Ford, B., Querfurth, H. 2003 Downregulation and increased turnover of b-Amyloid Precursor Protein in skeletal muscle cultures by Neuregulin. 2003 Exp. Neurol. 181; 170-180. [PubMed]

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