Bruce Trapp

Summary

Affiliation: Cleveland Clinic Foundation
Country: USA

Publications

  1. ncbi request reprint Axonal pathology in multiple sclerosis: relationship to neurologic disability
    B D Trapp
    Department of Neurosciences, Cleveland Clinic Foundation, Cleveland, OH 44195, USA
    Curr Opin Neurol 12:295-302. 1999
  2. pmc Evolution of a neuroprotective function of central nervous system myelin
    Xinghua Yin
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA
    J Cell Biol 172:469-78. 2006
  3. pmc Neurogenesis in the chronic lesions of multiple sclerosis
    Ansi Chang
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    Brain 131:2366-75. 2008
  4. doi request reprint Lessons from Jack Griffin and the "pathogenesis of peripheral nerve disease"
    Bruce D Trapp
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    J Peripher Nerv Syst 17:20-3. 2012
  5. pmc Heterophilic binding of L1 on unmyelinated sensory axons mediates Schwann cell adhesion and is required for axonal survival
    C A Haney
    Department of Neuroscience, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Cell Biol 146:1173-84. 1999
  6. ncbi request reprint Evidence for synaptic stripping by cortical microglia
    Bruce D Trapp
    Department of Neurosciences, Lerner Research Institute, The Cleveland Clinic, Cleveland, OH 44195, USA
    Glia 55:360-8. 2007
  7. ncbi request reprint Axonal degeneration and progressive neurologic disability in multiple sclerosis
    Carl Bjartmar
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195, USA
    Neurotox Res 5:157-64. 2003
  8. ncbi request reprint N-acetyl-L-aspartate in multiple sclerosis
    Gerson A Criste
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
    Adv Exp Med Biol 576:199-214; discussion 361-3. 2006
  9. doi request reprint Rescue of congenital hypomyelination by progenitor cell transplantation
    Bruce D Trapp
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    Cell Stem Cell 2:519-20. 2008
  10. ncbi request reprint Multiple sclerosis: an immune or neurodegenerative disorder?
    Bruce D Trapp
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA
    Annu Rev Neurosci 31:247-69. 2008

Research Grants

Collaborators

Detail Information

Publications54

  1. ncbi request reprint Axonal pathology in multiple sclerosis: relationship to neurologic disability
    B D Trapp
    Department of Neurosciences, Cleveland Clinic Foundation, Cleveland, OH 44195, USA
    Curr Opin Neurol 12:295-302. 1999
    ..Finally, studies of the time course of axonal loss, and its mechanisms are critical for effective therapeutic intervention...
  2. pmc Evolution of a neuroprotective function of central nervous system myelin
    Xinghua Yin
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA
    J Cell Biol 172:469-78. 2006
    ..These data support the hypothesis that the P0-PLP shift during vertebrate evolution provided a vital neuroprotective function to myelin-forming CNS glia...
  3. pmc Neurogenesis in the chronic lesions of multiple sclerosis
    Ansi Chang
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    Brain 131:2366-75. 2008
    ..These results support neurogenesis in a subpopulation of demyelinated subcortical white matter lesions in multiple sclerosis brains...
  4. doi request reprint Lessons from Jack Griffin and the "pathogenesis of peripheral nerve disease"
    Bruce D Trapp
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    J Peripher Nerv Syst 17:20-3. 2012
    ....
  5. pmc Heterophilic binding of L1 on unmyelinated sensory axons mediates Schwann cell adhesion and is required for axonal survival
    C A Haney
    Department of Neuroscience, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Cell Biol 146:1173-84. 1999
    ....
  6. ncbi request reprint Evidence for synaptic stripping by cortical microglia
    Bruce D Trapp
    Department of Neurosciences, Lerner Research Institute, The Cleveland Clinic, Cleveland, OH 44195, USA
    Glia 55:360-8. 2007
    ..Since neuronal pathology was not a feature of either the acute or immune-mediated lesion, synaptic stripping by activated microglia may have neuroprotective consequences...
  7. ncbi request reprint Axonal degeneration and progressive neurologic disability in multiple sclerosis
    Carl Bjartmar
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195, USA
    Neurotox Res 5:157-64. 2003
    ..Finally, surrogate markers of axonal pathology, such as N-acetyl aspartate, can be used to monitor axonal dysfunction, axonal loss and treatment efficiency in patients with MS...
  8. ncbi request reprint N-acetyl-L-aspartate in multiple sclerosis
    Gerson A Criste
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
    Adv Exp Med Biol 576:199-214; discussion 361-3. 2006
  9. doi request reprint Rescue of congenital hypomyelination by progenitor cell transplantation
    Bruce D Trapp
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    Cell Stem Cell 2:519-20. 2008
    ..In this issue of Cell Stem Cell, Windrem et al. (2008) describe the first progenitor cell transplantation paradigm that rescues the neurological phenotypes and increases life spans of mice with inherited myelin disease...
  10. ncbi request reprint Multiple sclerosis: an immune or neurodegenerative disorder?
    Bruce D Trapp
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA
    Annu Rev Neurosci 31:247-69. 2008
    ....
  11. ncbi request reprint Axonal and neuronal degeneration in multiple sclerosis: mechanisms and functional consequences
    C Bjartmar
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
    Curr Opin Neurol 14:271-8. 2001
    ..The view that MS can also be considered an inflammatory neurodegenerative disease has important clinical implications for therapeutic approaches, monitoring of patients, and future treatment strategies...
  12. ncbi request reprint Virtual hypoxia and chronic necrosis of demyelinated axons in multiple sclerosis
    Bruce D Trapp
    Department of Neurosciences, Cleveland Clinic, Cleveland, OH 44195, USA
    Lancet Neurol 8:280-91. 2009
    ..The development of neuroprotective therapies that target these mechanisms might constitute effective adjuncts to currently used immune-modifying agents...
  13. pmc Axo-glial septate junctions. The maestro of nodal formation and myelination?
    B D Trapp
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
    J Cell Biol 150:F97-F100. 2000
  14. pmc Imaging correlates of leukocyte accumulation and CXCR4/CXCL12 in multiple sclerosis
    Natalia M Moll
    Neuroinflammation Research Center, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    Arch Neurol 66:44-53. 2009
    ..We studied the following ROIs: normal-appearing white matter (NAWM); regions abnormal only on T2-weighted images (T2 only); and regions abnormal on T2- and T1-weighted images with an abnormal magnetization transfer ratio (T2/T1/MTR)...
  15. pmc Beta4 tubulin identifies a primitive cell source for oligodendrocytes in the mammalian brain
    Chuanshen Wu
    Department of Neurosciences, Lerner Research Institute and Anatomic Pathology, Cleveland Clinic, Cleveland, Ohio 44195, USA
    J Neurosci 29:7649-57. 2009
    ..We propose that betaT4 cells are an endogenous cell source that can be recruited to promote neural repair in the adult telencephalon...
  16. ncbi request reprint Imaging correlates of axonal swelling in chronic multiple sclerosis brains
    Elizabeth Fisher
    Department of Biomedical Engineering, Lerner Research Institute, Cleveland, OH 44195, USA
    Ann Neurol 62:219-28. 2007
    ....
  17. ncbi request reprint The 36K protein of zebrafish CNS myelin is a short-chain dehydrogenase
    Jacqueline K Morris
    Department of Neurosciences, Cleveland Clinic Foundation, Lerner Research Institute, Cleveland, Ohio 44195, USA
    Glia 45:378-91. 2004
    ..This study identified a major myelin protein in zebrafish, 36K, as a member of the SDR superfamily; an expression pattern similar to other myelin genes was demonstrated...
  18. ncbi request reprint The tetraspanin protein, CD9, is expressed by progenitor cells committed to oligodendrogenesis and is linked to beta1 integrin, CD81, and Tspan-2
    Nobuo Terada
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
    Glia 40:350-9. 2002
    ..These data support the hypothesis that CD9 helps form the tetraspanin web beneath the plasma membranes of progenitor cells committed to oligodendrogenesis, but that CD9 is not essential for oligodendrogenesis and myelination...
  19. ncbi request reprint Taking two TRAILS
    Richard M Ransohoff
    Department of Neurosciences, Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
    Neuron 46:355-6. 2005
    ..This report poses the therapeutic challenge of facilitating TRAIL expression in the periphery while inhibiting TRAIL in the CNS...
  20. ncbi request reprint N-acetylaspartate is an axon-specific marker of mature white matter in vivo: a biochemical and immunohistochemical study on the rat optic nerve
    Carl Bjartmar
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA
    Ann Neurol 51:51-8. 2002
    ..In addition, the results indicate that neuronal adaptation can increase N-acetylaspartate levels, and that 5 to 20% of the N-acetylaspartate in developing white matter is synthesized by proliferating oligodendrocyte progenitor cells...
  21. ncbi request reprint Axon loss in the spinal cord determines permanent neurological disability in an animal model of multiple sclerosis
    Jerome R Wujek
    Department of Neurosciences NC30, Lerner Research Institute, Cleveland Clinic Foundation, Ohio 44195, USA
    J Neuropathol Exp Neurol 61:23-32. 2002
    ..This chronic-relapsing EAE model provides an excellent platform for 2 critical objectives: investigating mechanisms of axon loss and evaluating efficacy of neuroprotective therapies...
  22. ncbi request reprint Pathogenesis of axonal and neuronal damage in multiple sclerosis
    Ranjan Dutta
    Department of Neuroscience, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    Neurology 68:S22-31; discussion S43-54. 2007
    ..Therapeutic interventions directed toward each of these mechanisms need to be tested for their efficacy in enhancing axon survival and, ultimately, their ability to delay progression of neurologic disability in patients with MS...
  23. ncbi request reprint Treatment of experimental autoimmune encephalomyelitis with the chemokine receptor antagonist Met-RANTES
    Masaru Matsui
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA
    J Neuroimmunol 128:16-22. 2002
    ..Further analysis of the effects of chemokine receptor blockade may need to focus on leukocyte activation within the affected CNS as well as trafficking events...
  24. pmc P0 protein is required for and can induce formation of schmidt-lantermann incisures in myelin internodes
    Xinghua Yin
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA
    J Neurosci 28:7068-73. 2008
    ..These data support the hypotheses that P(0) protein is required for and can induce S-L incisures and that P(0)-induced CNS incisures can be detrimental to axonal function...
  25. ncbi request reprint Premyelinating oligodendrocytes in chronic lesions of multiple sclerosis
    Ansi Chang
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA
    N Engl J Med 346:165-73. 2002
    ..We investigated the frequency distribution and configuration of oligodendrocytes in chronic lesions of multiple sclerosis to determine whether these factors limit remyelination...
  26. doi request reprint NG2-positive glia in the human central nervous system
    Susan M Staugaitis
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    Neuron Glia Biol 5:35-44. 2009
    ..Advances in our understanding of NG2 glia in human tissues will require the development of more robust markers for their detection in routinely processed human specimens...
  27. pmc Demyelination increases axonal stationary mitochondrial size and the speed of axonal mitochondrial transport
    Sumiko Kiryu-Seo
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA
    J Neurosci 30:6658-66. 2010
    ..In response to insufficient ATP production, demyelinated axons increase the size of stationary mitochondrial sites and thereby balance ATP production with the increased energy needs of nerve conduction...
  28. ncbi request reprint Beta IV tubulin is selectively expressed by oligodendrocytes in the central nervous system
    Nobuo Terada
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
    Glia 50:212-22. 2005
    ..Beta(IV) tubulin may play a role in establishing the oligodendrocyte MT network, which is essential for the transport of myelin proteins, lipids, and RNA during myelination...
  29. ncbi request reprint Mitochondrial dysfunction as a cause of axonal degeneration in multiple sclerosis patients
    Ranjan Dutta
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, OH 44195, USA
    Ann Neurol 59:478-89. 2006
    ..Development of neuroprotective therapies will require elucidation of the molecular mechanisms by which neurons and axons degenerate...
  30. ncbi request reprint Bace1 modulates myelination in the central and peripheral nervous system
    Xiangyou Hu
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, Ohio 44195, USA
    Nat Neurosci 9:1520-5. 2006
    ..Based upon these and previous studies, we postulate that neuronally enriched Bace1 cleaves neuregulin-1 and that processed neuregulin-1 regulates myelination by means of phosphorylation of Akt in myelin-forming cells...
  31. ncbi request reprint VCAM-1-positive microglia target oligodendrocytes at the border of multiple sclerosis lesions
    John W Peterson
    Department of Neurosciences, Lerner Research Institute, The Cleveland Clinic Foundation, Ohio 44195, USA
    J Neuropathol Exp Neurol 61:539-46. 2002
    ..Endothelial cells were VCAM-1-negative in both lesion and non-lesion MS brain tissue. This report is the first to document direct microglial interaction with oligodendrocytes in MS...
  32. ncbi request reprint Activation of the ciliary neurotrophic factor (CNTF) signalling pathway in cortical neurons of multiple sclerosis patients
    Ranjan Dutta
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    Brain 130:2566-76. 2007
    ..Induction of CNTF signalling and the anti-apoptotic molecule, Bcl2, thus represents a compensatory response to disease pathogenesis and a potential therapeutic target in MS patients...
  33. pmc Genetic deletion of BACE1 in mice affects remyelination of sciatic nerves
    Xiangyou Hu
    Department of Neurosciences, Lerner Research Institute, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195, USA
    FASEB J 22:2970-80. 2008
    ..Pharmacological inhibition of BACE1 should be carefully monitored to avoid alteration of signaling pathway that regulates remyelination...
  34. ncbi request reprint Oligodendrogenesis is differentially regulated in gray and white matter of jimpy mice
    Karen L Baracskay
    Department of Neuroscience, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA
    J Neurosci Res 70:645-54. 2002
    ..These data provide additional evidence that oligodendrogenesis is differentially regulated in white matter and gray matter and implicate PLP/DM20 as a modulator of these differences...
  35. ncbi request reprint Preconditioning paradigms and pathways in the brain
    Karl B Shpargel
    Department of Neurosciences, Cleveland Clinic Foundation, Cleveland, OH 44195, USA
    Cleve Clin J Med 75:S77-82. 2008
    ..Elucidation of the endogenous cell survival pathways involved in preconditioning has significant clinical implications for preventing neuronal damage in susceptible patients...
  36. ncbi request reprint Neuropathobiology of multiple sclerosis
    John W Peterson
    Department of Neurosciences, The Lerner Research Institute, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA
    Neurol Clin 23:107-29, vi-vii. 2005
  37. doi request reprint Imaging correlates of decreased axonal Na+/K+ ATPase in chronic multiple sclerosis lesions
    Elizabeth A Young
    Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH, USA
    Ann Neurol 63:428-35. 2008
    ..To date, however, the distribution of Na+/K+ ATPase has not been studied in MS lesions...
  38. ncbi request reprint NG2-positive cells generate A2B5-positive oligodendrocyte precursor cells
    Karen L Baracskay
    Department of Neuroscience, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA
    Glia 55:1001-10. 2007
    ..NG2(+) cells appear prior to the expression of A2B5(+) cells and generate A2B5(+) cells. We propose that during development NG2(+)/A2B5(-) cells (pre-OPCs) represent the direct ancestor to A2B5(+) O2A progenitor cells (OPCs)...
  39. ncbi request reprint Dysmyelinated lower motor neurons retract and regenerate dysfunctional synaptic terminals
    Xinghua Yin
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
    J Neurosci 24:3890-8. 2004
    ..Maintenance of synaptic connections should be considered as a therapeutic target for slowing progression of neurological disability in primary diseases of myelin...
  40. ncbi request reprint [Pathology and definition of multiple sclerosis]
    Ranjan Dutta
    Department of Neuroscience, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
    Rev Prat 56:1293-8. 2006
    ..disease, and Devic's acute neuromyelitis optica or are there distinct nosological entities? As for autoimmunisation which leads to the selective destruction of myelin, is it primary or secondary to an oligodendrocytic apoptotic process?..
  41. ncbi request reprint Expression of protein 4.1G in Schwann cells of the peripheral nervous system
    Nobuhiko Ohno
    Department of Anatomy, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo City, Yamanashi, Japan
    J Neurosci Res 84:568-77. 2006
    ..These data support the concept that 4.1G plays an important role in the membrane expansion and specialization that occurs during formation and maintenance of myelin internodes in the peripheral nervous system...
  42. ncbi request reprint Subpial demyelination in the cerebral cortex of multiple sclerosis patients
    Lars Bø
    Department of Neurology, Haukeland Hospital, Bergen, Norway
    J Neuropathol Exp Neurol 62:723-32. 2003
    ..05). These results indicate that the cerebral cortex is likely to be a predilection site for MS lesions and identify general cortical subpial demyelination as a distinct pattern occurring in a significant subpopulation of MS patients...
  43. ncbi request reprint Neurodegeneration and neuroprotection in multiple sclerosis and other neurodegenerative diseases
    Suhayl Dhib-Jalbut
    UMDNJ Robert Wood Johnson Medical School, New Brunswick, NJ 08901, and The Cleveland Clinic, OH, USA
    J Neuroimmunol 176:198-215. 2006
    ..Elucidating the mechanisms that orchestrate neuronal diseases should facilitate development of neuroprotective and neurorestorative strategies...
  44. ncbi request reprint Hyaluronan accumulates in demyelinated lesions and inhibits oligodendrocyte progenitor maturation
    Stephen A Back
    Department of Pediatrics, School of Medicine, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, Oregon 97239, USA
    Nat Med 11:966-72. 2005
    ..HMW hyaluronan may therefore contribute substantially to remyelination failure by preventing the maturation of OPCs that are recruited to demyelinating lesions...
  45. ncbi request reprint Structure and stability of internodal myelin in mouse models of hereditary neuropathy
    Robin L Avila
    Biology Department, Boston College, Chestnut Hill, MA 02467, USA
    J Neuropathol Exp Neurol 64:976-90. 2005
    ..Our findings demonstrate that diffraction can provide a quantitative basis for understanding, at a molecular level, the membrane packing defects that occur in internodal myelin in demyelinating peripheral neuropathies...
  46. ncbi request reprint Oligodendrocyte precursor hypercellularity and abnormal retina development in mice overexpressing PDGF-B in myelinating tracts
    Karin Forsberg-Nilsson
    Department of Genetics and Pathology, Rudbeck Laboratory, Uppsala, Sweden
    Glia 41:276-89. 2003
    ..Our observations strengthen the notion that PDGF is an important effector molecule in postnatal CNS development...
  47. ncbi request reprint Pathogenesis of multiple sclerosis: the eyes only see what the mind is prepared to comprehend
    Bruce D Trapp
    Ann Neurol 55:455-7. 2004
  48. pmc Relating interactions between neurofilaments to the structure of axonal neurofilament distributions through polymer brush models
    Sanjay Kumar
    Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Biophys J 82:2360-72. 2002
    ..The presence of attractive cross-bridging interactions contributes only modestly to structure for moderate degrees of cross-bridging and leads to NF aggregation for extensive cross-bridging...
  49. ncbi request reprint Role of long-range repulsive forces in organizing axonal neurofilament distributions: evidence from mice deficient in myelin-associated glycoprotein
    Sanjay Kumar
    Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci Res 68:681-90. 2002
    ..Among the models tested, a model in which the filaments interact through a long-range repulsive force is most consistent with the results of our analysis...
  50. ncbi request reprint The neuroprotective factor Wlds does not attenuate mutant SOD1-mediated motor neuron disease
    Christine Vande Velde
    Ludwig Institute for Cancer Research and Departments of Medicine and Neuroscience, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA
    Neuromolecular Med 5:193-203. 2004
    ..However, presynaptic endings in both the presence and absence of Wld(s) showed high accumulations of mitochondria and synaptic vesicles, implicating errors of retrograde transport as a consequence of SOD1-mutant damage to axons...
  51. ncbi request reprint Axon-glial signaling and the glial support of axon function
    Klaus Armin Nave
    Department of Neurogenetics, Max Planck Institute of Experimental Medicine, D 37075 Gottingen, Germany
    Annu Rev Neurosci 31:535-61. 2008
    ..Loss of glial support causes progressive axon degeneration and possibly local inflammation, both of which are likely to contribute to a variety of neuronal diseases in the central and peripheral nervous systems...
  52. ncbi request reprint Sodium channel expression within chronic multiple sclerosis plaques
    Joel A Black
    Department of Neurology and Paralyzed Veterans of America United Spinal Association Neuroscience Research Center, Yale University School of Medicine, New Haven, CT, USA
    J Neuropathol Exp Neurol 66:828-37. 2007
    ..6 and NCX in acute lesions but independent of coexpression of these 2 molecules in chronic lesions...

Research Grants34

  1. CELLULAR MECHANISMS OF OLIGODENDROCYTE MYELINATION
    Bruce Trapp; Fiscal Year: 2004
    ....
  2. Pathogenesis in Demyelination of MS Brains
    Bruce D Trapp; Fiscal Year: 2010
    ..We will study MS patients with reduced memory, develop brain imaging techniques to identify MS patients at risk for memory problems and identify ways to treat MS patients with memory loss. ..
  3. PATHOGENESIS OF DEMYELINATION IN MS BRAINS
    Bruce Trapp; Fiscal Year: 2003
    ..Collectively, our studies should identify new targets for therapeutic intervention that will reduce and delay neurodegeneration and the progression of permanent neurological disability in MS patients. ..
  4. CELLULAR MECHANISMS OF OLIGODENDROCYTE MYELINATION
    Bruce Trapp; Fiscal Year: 2003
    ....
  5. PATHOGENESIS OF DEMYELINATION IN MS BRAINS
    Bruce Trapp; Fiscal Year: 2004
    ..Collectively, our studies should identify new targets for therapeutic intervention that will reduce and delay neurodegeneration and the progression of permanent neurological disability in MS patients. ..
  6. PATHOGENESIS OF DEMYELINATION IN MS BRAINS
    Bruce Trapp; Fiscal Year: 2005
    ..Collectively, our studies should identify new targets for therapeutic intervention that will reduce and delay neurodegeneration and the progression of permanent neurological disability in MS patients. ..
  7. Cellular Mechanisms for Oligodendrocyte Myelination
    Bruce Trapp; Fiscal Year: 2006
    ..Collectively, these studies should identify therapeutic targets that enhance remyelination and reduce the progression of neurological disability in MS patients. ..
  8. Cellular Mechanisms for Oligodendrocyte Myelination
    Bruce Trapp; Fiscal Year: 2007
    ..Collectively, these studies should identify therapeutic targets that enhance remyelination and reduce the progression of neurological disability in MS patients. ..
  9. MOLECULAR MECHANISMS OF SCHWANN CELL MYELINATION
    Bruce Trapp; Fiscal Year: 2007
    ....
  10. Cellular Mechanisms for Oligodendrocyte Myelination
    Bruce Trapp; Fiscal Year: 2009
    ..Collectively, these studies should identify therapeutic targets that enhance remyelination and reduce the progression of neurological disability in MS patients. ..
  11. Pathogenesis in Demyelination of MS Brains
    Bruce Trapp; Fiscal Year: 2009
    ..We will study MS patients with reduced memory, develop brain imaging techniques to identify MS patients at risk for memory problems and identify ways to treat MS patients with memory loss. ..
  12. MOLECULAR MECHANISMS OF SCHWANN CELL MYELINATION
    Bruce D Trapp; Fiscal Year: 2010
    ..The results will contribute to understanding myelin disease pathology and provide clues for effective future therapeutic strategies for treating primary myelin diseases. ..
  13. Cellular Mechanisms for Oligodendrocyte Myelination
    Bruce D Trapp; Fiscal Year: 2010
    ..Collectively, these studies should identify therapeutic targets that enhance remyelination and reduce the progression of neurological disability in MS patients. ..
  14. CELLULAR MECHANISMS OF OLIGODENDROCYTE MYELINATION
    Bruce Trapp; Fiscal Year: 2002
    ....
  15. PATHOGENESIS OF DEMYELINATION IN MS BRAINS
    Bruce Trapp; Fiscal Year: 2002
    ..Collectively, our studies should identify new targets for therapeutic intervention that will reduce and delay neurodegeneration and the progression of permanent neurological disability in MS patients. ..
  16. MOLECULAR MECHANISMS OF SCHWANN CELL MYELINATION
    Bruce Trapp; Fiscal Year: 1999
    ..abstract_text> ..
  17. PATHOGENESIS OF DEMYELINATION IN MS BRAINS
    Bruce Trapp; Fiscal Year: 1999
    ..If it can be demonstrated that these molecules play an essential role in leukocyte trafficking, they become attractive targets for therapeutic intervention in MS. ..
  18. CELLULAR MECHANISMS OF OLIGODENDROCYTE MYELINATION
    Bruce Trapp; Fiscal Year: 1999
    ....
  19. PATHOGENESIS OF DEMYELINATION IN MS BRAINS
    Bruce Trapp; Fiscal Year: 2000
    ..If it can be demonstrated that these molecules play an essential role in leukocyte trafficking, they become attractive targets for therapeutic intervention in MS. ..
  20. MOLECULAR MECHANISMS OF SCHWANN CELL MYELINATION
    Bruce Trapp; Fiscal Year: 2000
    ..abstract_text> ..
  21. CELLULAR MECHANISMS OF OLIGODENDROCYTE MYELINATION
    Bruce Trapp; Fiscal Year: 2000
    ....
  22. MOLECULAR MECHANISMS OF SCHWANN CELL MYELINATION
    Bruce Trapp; Fiscal Year: 2001
    ..abstract_text> ..
  23. CELLULAR MECHANISMS OF OLIGODENDROCYTE MYELINATION
    Bruce Trapp; Fiscal Year: 2001
    ....