Matthew Harms, MD
Dr. Harms’ laboratory investigates the genetic landscape of amyotrophic lateral sclerosis (ALS) and a range of other hereditary neuromuscular diseases that includes CMT, SMA, and LGMD. These efforts use next-generation sequencing technology to understand the mutational spectrum of known genes in these diseases, but focus strongly on novel gene discovery. Using exome sequencing, Dr. Harms’ team has discovered that mutations inDYNC1H1are the cause of an autosomal dominant form of spinal muscular atrophy, and that limb-girdle muscular dystrophy 1D results from abnormalities ofDNAJB6. His lab is now leveraging their next-gen expertise to identify additional genes for ALS, hoping to provide insights into disease pathology and identify therapeutic targets.
Dr. Harms' clinical activities focus on the evaluation and treatment of patients with neuromuscular disease, including amyotrophic lateral sclerosis, neuropathy, myopathy, and myasthenia gravis. He also participates as an investigator for clinical trials in these diseases, and performs electromyography/nerve conduction studies.
Dr. Harms, MD received his B.A. in biologysumma cum laudefrom Harvard University in 1997, where his coursework and thesis focused on the neurosciences. After completing additional neurobiology research in the lab of Liqun Luo, PhD at Stanford University, he attended medical school at the University of California, San Francisco. He received his medical degree with AOA honors in 2003 and stayed to complete residency. In 2007, Dr. Harms came to Washington University for fellowship training in clinical neurophysiology and neuromuscular medicine, during which he carried out genetics research in the lab of Bob Baloh. He joined the Department of Neurology faculty in 2009 and is a member of the Hope Center for Neurological Disorders.
Harms MB, Cady J, Zaidman C, Cooper P, Bali T, Allred P, Cruchaga C, Baughn M, Pestronk A, Goate A, Ravits R, Baloh RH. Lack of C9ORF72 coding mutations supports a gain of function for repeats expansions in ALS. Neurobiology of Aging 2013.In press.
Harms MB, Benitez B, Cairns N, Cooper B, Cooper P, Mayo K, Carrell D, Faber K, Williamson J, Bird T, Diaz-Arrastia R, Foroud TM, Boeve BF, Graff-Radford NR, Mayeux R, Chakraverty S, Goate A, and Cruchaga C. C9ORF72 hexanucleotide repeat expansions in clinical Alzheimer’s disease. AMA Neurol. 2013(1-6). doi:10.1001/2013.jamaneurol.537. Online April 15, 2013.
Harms MB, Neumann D, Benitez B, Cooper B, Racette BA, Perlmutter JS, Goate AB, Cruchaga C*. Parkinson Disease is not associated with C9ORF72 repeat expansions. Neurobiology of Aging. 2013 May;34(5):1519.e1-2. On-line Oct. 30, 2012.
Harms MB, Sommerville RB, Allred P, Bell S, Ma D, Cooper P, Lopate G, Pestronk A, Weihl CC, Baloh RH. Exome sequencing revealsDNAJB6mutations in dominantly-inherited myopathy. Annals of Neurology 2012 Mar;71(3):407-16. On-line Feb 14,2012.
Harms MB, Ori-McKenney KM, Scoto M, Tuck E, Bell S, Ma D, Masi S, Allred P, Al-Lozi M, Reilly M, Miller LJ, Jani-Ascadi A, Pestronk A, Shy ME, Muntoni F, Vallee RB, Baloh RH. Mutations in the tail domain ofDYNC1H1cause dominant spinal muscular atrophy. Neurology 2012 May 29;78(22):1714-20. On-line Mar 28, 2012.
Harms MB, Allred P, Gardner R, Fernandes Filho JA, Florence J, Pestronk A, Al-Lozi M, Baloh RH. Dominant spinal muscular atrophy with lower extremity predominance: Linkage to 14q32. Neurology 2010 75: 7539-546.
Ng J, Nardine T, Harms MB, Tzu J, Goldstein A, Sun Y, Dietzl G, Dickson BJ, Luo L. Rac GTPases control axon growth, guidance and branching. Nature 2002;416: 442-7.
Hakeda-Suzuki S, Ng J, Tzu J, Dietzl G, Sun Y, Harms MB, Nardine T, Luo L, Dickson BJ. Rac function and regulation during Drosophila development. Nature 2002 416: 438-42.
Nakayama AY, Harms MB, Luo L. Small GTPases Rac and Rho in the maintenance of dendritic spines and branches in hippocampal pyramidal neurons. J Neuroscience 2000 20: 5329-38.
Pawlikowska L, Cottrell SE, Harms MB, Li Y, Rosenberg PA. Extracellular synthesis of cADP-ribose from nicotinamide-adenine dinucleotide by rat cortical astrocytes in culture. J Neurosci 1996 16: 5372-81.
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