Bruce D Trapp, Ph.D.
Staff and Department Chair
The Morris R. and Ruth V. Graham Endowed Chair in Biomedical Research
Professor, Molecular Medicine, CCLCM-CWRU
Lerner Research Institute,
9500 Euclid Avenue, Cleveland, Ohio 44195
Phone: (216) 444-7177
Fax: (216) 444-7927
Our research aims are to obtain a better understanding of cellular/molecular events involved in glial cell development and myelin formation in the central and peripheral nervous systems (CNS and PNS) and to understand how myelin, myelin-forming cells, and axons are destroyed in autoimmune and inherited diseases of myelin.
New data about the normal functioning of myelin-forming cells and myelin-axon interactions will help us understand the pathogenic mechanisms involved in permanent neurological disability in human diseases of myelin.
Cellular/Molecular Biology of Myelination: Our aim is to obtain a better understanding of cellular/molecular events that regulate production and differentiation of oligodendrocytes and CNS myelination. Using transgenic mice, we study the role of myelin and myelin proteins in maintaining axonal function and survival. We also investigate the role ofCNS progenitor cells as a source of new oligodendrocytes in the adult brain.
Pathogenesis of Neurological Disability in Multiple Sclerosis (MS): In these studies, we seek to determine the causes of MS, an inflammatory demyelinating disease of the CNS, and to therapeutically preventirreversible neurological disability in MS patients. Historically, it has been assumed that axons were spared most of the pathological consequences of inflammatory demyelination. We have described axonal degeneration during demyelination and as a result of chronic demyelination. We also focus on neuronal degeneration and axonal pathology in the cerebral cortex and hippocampus of MS patients. Recent studies also focus on the therapeutic potential of progenitor cells to repair demyelinated or dysmyelinated brain.
Selected Publications (2014-present):
Trapp BD, Ontaneda D. (2018) Identifying a new subtype of multiple sclerosis. Neurodegener Dis Manag. 8(6):367-369.PMID: 30215581
Trapp BD, Vignos M, Dudman J, Chang A, Fisher E, Staugaitis SM, Battapady H, Mork S, Ontaneda D, Jones SE, Fox RJ, Chen J, Nakamura K, Rudick RA. (2018) Cortical neuronal densities and cerebral white matter demyelination in multiple sclerosis: a retrospective study. Lancet Neurol. 17(10):870-884. PMID: 30143361
Dutta R, Trapp BD. (2018) Much, if not all, of the cortical damage in MS can be attributed to the microglial cell - No. Mult Scler. 24(7):897-899. PMID: 29754529; PMCID: PMC5995597
Koenig KA, Rao SM, Lowe MJ, Lin J, Sakaie KE, Stone L, Bermel RA, Trapp BD, Phillips MD. (2018) The role of the thalamus and hippocampus in episodic memory performance in patients with multiple sclerosis. Mult Scler. Mar 1:1352458518760716. PMID: 29512427
He X, Zhang L, Queme LF, Liu X, Lu A, Waclaw RR, Dong X, Zhou W, Kidd G, Yoon SO, Buonanno A, Rubin JB, Xin M, Nave KA, Trapp BD, Jankowski MP, Lu QR. (2018) A histone deacetylase 3-dependent pathway delimits peripheral myelin growth and functional regeneration. Nat Med. 24(3):338-351. PMID: 29431744; PMCID: PMC5908710
Chen J, Kostenko V, Pioro EP, Trapp BD. (2018) MR Imaging-based Estimation of Upper Motor Neuron Density in Patients with Amyotrophic Lateral Sclerosis: A Feasibility Study. Radiology 287(3):955-964. PMID: 29361242; PMCID: PMC5978454
Jawaid S, Kidd GJ, Wang J, Swetlik C, Dutta R, Trapp BD. (2018) Alterations in CA1 hippocampal synapses in a mouse model of fragile X syndrome. Glia 66(4):789-800. PMID: 29274095; PMCID: PMC5812820
Nakamura K, Chen JT, Ontaneda D, Fox RJ, Trapp BD. (2017) T1-/T2-weighted ratio differs in demyelinated cortex in multiple sclerosis. Ann Neurol. 82(4):635-639. PMID: 28833377
Chomyk AM, Volsko C, Tripathi A, Deckard SA, Trapp BD, Fox RJ, Dutta R. (2017) DNA methylation in demyelinated multiple sclerosis hippocampus. Sci Rep. 7(1):8696. PMID: 28821749; PMCID: PMC5562763
Yin X, Kidd GJ, Ohno N, Perkins GA, Ellisman MH, Bastian C, Brunet S, Baltan S, Trapp BD. (2016) Proteolipid protein-deficient myelin promotes axonal mitochondrial dysfunction via altered metabolic coupling. J Cell Biol. 215(4):531-542. PMID: 27872255; PMCID: PMC5119941
Bai CB, Sun S, Roholt A, Benson E, Edberg D, Medicetty S, Dutta R, Kidd G, Macklin WB, Trapp B. (2016) A mouse model for testing remyelinating therapies. Exp Neurol. 283(Pt A):330-340. PMID: 27384502; PMCID: PMC5207347
Chen Z, Chen JT, Johnson M, Gossman ZC, Hendrickson M, Sakaie K, Martinez-Rubio C, Gale JT, Trapp BD. (2015) Cuprizone does not induce CNS demyelination in nonhuman primates. Ann Clin Transl Neurol. 2:208-13. PMID: 25750925; PMCID: PMC4338961
Mahad DH, Trapp BD, Lassmann H. (2015) Pathological mechanisms in progressive multiple sclerosis. Lancet Neurol. 14:183-93. PMID: 25772897
Yin X, Kiryu-Seo S, Kidd GJ, Feltri ML, Wrabetz L, Trapp BD. (2015) Proteolipid protein cannot replace P0 protein as the major structural protein of peripheral nervous system myelin. Glia 63:66-77. PMID: 25066805; PMCID: PMC4237650
Chiang H, Ohno N, Hsieh YL, Mahad DJ, Kikuchi S, Komuro H, Hsieh ST, Trapp BD. (2015) Mitochondrial fission augments capsaicin-induced axonal degeneration. Acta Neuropathol. 129:81-96. PMID: 25322817; PMCID: PMC4282704
Chen Z, Jalabi W, Hu W, Park HJ, Gale JT, Kidd GJ, Bernatowicz R, Gossman ZC, Chen JT, Dutta R, Trapp BD. (2014) Microglial displacement of inhibitory synapses provides neuroprotection in the adult brain. Nat Commun. 22:4486-97. PMID: 25047355; PMCID: PMC4109015
Ohno N, Chiang H, Mahad DJ, Kidd GJ, Liu L, Ransohoff RM, Sheng ZH, Komuro H, Trapp BD. (2014) Mitochondrial immobilization mediated by syntaphilin facilitates survival of demyelinated axons. Proc Natl Acad Sci USA. 111:9953-58. PMID: 24958879; PMCID: PMC4103317
Dutta R, Trapp BD. (2014) Relapsing and progressive forms of multiple sclerosis: insights from pathology. Curr Opin Neurol. 27:271-78. PMID: 24722325; PMCID: PMC4132635
Huynh JL, Garg P, Thin TH, Yoo S, Dutta R, Trapp BD, Haroutunian V, Zhu J, Donovan MJ, Sharp AJ, Casaccia P. (2014) Epigenome-wide differences in pathology-free regions of multiple sclerosis-affected brains. Nat Neurosci. 17:121-30. PMID: 24270187; PMCID: PMC3934491
|US Patent||Patent Title||Issue Date||First-Named Inventor|
Multipotent neural stem cells
September 28, 2010
Multipotent neural stem cells
February 26, 2013
Cleveland Clinic researchers have discovered a new subtype of multiple sclerosis (MS), providing a better understanding of the individualized nature of the disease.
Cleveland Clinic researchers have discovered for the first time that faulty connections between nerve cells (neurons) causes Fragile X Syndrome (FXS), the leading inherited cause of intellectual disability and autism spectrum disorders. FXS is caused by mutations that silence the FMR1 gene (Fragile X Mental Retardation 1).
Bruce D. Trapp, PhD, an expert in multiple sclerosis (MS) and myelin biology, received an R35 Outstanding Investigator Award from the National Institutes of Health. The prestigious award is designed to provide long-term support and flexibility to scientists whose work holds the most promise for significant breakthroughs.