Skip to Content
Director of NeuropathologyCo-Director, Wellstone Muscular Dystrophy Cooperative Research CenterProfessor of Pathology
- Anatomic and Clinical Pathology
Primary Office: 5239B Roy Carver PavilionIowa City, IA 52242
Primary Office Phone: 319-384-9084
Lab: 4270A Carver Biomedical Research BuildingIowa City, IA 52242
Email: firstname.lastname@example.orgWeb: Muscular Dystrophy Diagnostic ServiceWeb: Dr. Moore's Research Laboratory
BS, Purdue UniversityPhD, Anatomy, Indiana UniversityMD, Indiana University School of Medicine
Residency, University of Iowa College of MedicineFellowship, University of Iowa College of Medicine
Anatomic Pathology, American Board of PathologyNeuropathology, American Board of Pathology
Biosciences Graduate ProgramDepartment of Pathology Graduate ProgramInterdisciplinary Graduate Program in Neuroscience
Muscular dystrophies are a diverse group of inherited disorders characterized by progressive muscle weakness and wasting. Dr. Moore is involved in the evaluation of patient biopsies and in research partially funded through a center grant from NIH. This Paul D. Wellstone Muscular Dystrophy Cooperative Research Center is exploring therapeutic strategies for the treatment of various muscular dystrophies by enabling translational research on muscular dystrophies and providing advanced diagnostic services. The MDCRC is composed of two research projects, three cores and investigators with a proven track record of excellence and collaboration. The Center researchers' studies and facilities will explore basic biological mechanisms that relate to possible treatments for muscular dystrophies, facilitate translational research on muscular dystrophies and provide advanced diagnostic services to patients and clinical trial participants. The Director and Co-director, Kevin Campbell and Steven Moore, are investigators with established records in basic, translational, and clinical research on muscular dystrophy.
Additional basic science collaboration with Dr. Kevin Campbell, Department of Molecular Physiology and Biophysics ( The Laboratory of Dr. Kevin P. Campbell) involves the pathologic characterization of genetic mouse models of muscular dystrophy. Many of these models use Cre-lox methodology to selectively knock out brain or peripheral nerve dystroglycan. These mice model congenital muscular dystrophy. A second basic science collaboration is with Lori Wallrath (Department of Biochemistry, The University of Iowa) studying lamin A/C.
Including the Wellstone MDCRC mentioned above, clinical diagnostic work in the general area of muscular dystophies has expanded into basic and clinical research projects in collaboration with several physicians at other institutions, Kevin Campbell, and Kathy Mathews (Department of Pediatrics, The University of Iowa). Current clinical studies involve: (1) a natural history study of patients with dystroglycanopathy, (2) a search for new genes in congenital myopathy and muscular dystrophy patients, (3) dysferlinopathy patients with amyloid deposition, (4) autophagic vacuolar myopathy patients, and (5) improvements in diagnostic testing.
Center for Gene Therapy of Cystic Fibrosis and other Genetic DiseasesSenator Paul D. Wellstone Muscular Dystrophy Cooperative Research Center
Differential Activation of catalase expression and activity by PPAR agonists: implications for astrocyte protection in anti-glioma therapy.
2013 January 26. 1(1):70-79.
von der Hagen J,
Novel deletion of lysine 7 expands the clinical, histopathologic and genetic spectrum of TPM2-related myopathies.
ISPD Gene Mutations are a common cause of congenital and limb-girdle muscular dystrophies.
2013 January. 136(Pt 1):269-81.
Sudden death and myocardial lesions after damage to catecholamine neurons of the nucleus tractus solitarii in rat.
Cellular Mol Neurobiol.
2012 October. 32(7):1119-26.
Le Rumeur E,
A novel mutation in spectrin-like repeat 1 of dystrophin central domain causes protein misfolding and mild Becker muscular dystrophy.
J Biol Chem.
2012 May. 287(22):18153-62.
de Bernabe D,
ISPD loss-of-function mutations disrupt dystroglycan O-mannosylation and cause Walker-Warburg syndrome.
2012 May. 44(5):575-80.
LMNA variants cause cytoplasmic distribution of nuclear pore proteins in Drosophila and human muscle.
Human Molecular Genetics.
2012 April. 21(7):1544-56.
CaMKII determines mitochondrial stress responses in heart.
Dystroglycan on radial glia end feet is required for pial basement membrane integrity and columnar organization of the developing cerebral cortex.
J Neuropathol Exp Neurol.
Date Last Modified: 06/07/2014 -
Copyright © 2011 The University of Iowa. All Rights Reserved.