Lee Martin

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. pmc The olfactory bulb in newborn piglet is a reservoir of neural stem and progenitor cells
    Lee J Martin
    Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America Pathobiology Graduate Program, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America The Solomon Snyder Department of Neuroscience Graduate Program, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
    PLoS ONE 8:e81105. 2013
  2. doi request reprint The mitochondrial permeability transition pore regulates Parkinson's disease development in mutant α-synuclein transgenic mice
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA Pathobiology Graduate Program, Johns Hopkins University School of Medicine, Baltimore, MD, USA Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA Electronic address
    Neurobiol Aging 35:1132-52. 2014
  3. pmc Aberrant regulation of DNA methylation in amyotrophic lateral sclerosis: a new target of disease mechanisms
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, 558 Ross Building, 720 Rutland Avenue, Baltimore, MD, 21205 2196, USA
    Neurotherapeutics 10:722-33. 2013
  4. pmc Nuclear localization of human SOD1 and mutant SOD1-specific disruption of survival motor neuron protein complex in transgenic amyotrophic lateral sclerosis mice
    Barry Gertz
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neuropathol Exp Neurol 71:162-77. 2012
  5. ncbi request reprint Adult olfactory bulb neural precursor cell grafts provide temporary protection from motor neuron degeneration, improve motor function, and extend survival in amyotrophic lateral sclerosis mice
    Lee J Martin
    Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neuropathol Exp Neurol 66:1002-18. 2007
  6. pmc Generation and characterization of transgenic mice expressing mitochondrial targeted red fluorescent protein selectively in neurons: modeling mitochondriopathy in excitotoxicity and amyotrophic lateral sclerosis
    Yi Wang
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, MD 21205, USA
    Mol Neurodegener 6:75. 2011
  7. pmc Olesoxime, a cholesterol-like neuroprotectant for the potential treatment of amyotrophic lateral sclerosis
    Lee J Martin
    Johns Hopkins University School of Medicine, Departments of Pathology and Neuroscience, Baltimore, MD 21205 2196, USA
    IDrugs 13:568-80. 2010
  8. pmc An approach to experimental synaptic pathology using green fluorescent protein-transgenic mice and gene knockout mice to show mitochondrial permeability transition pore-driven excitotoxicity in interneurons and motoneurons
    Lee J Martin
    Department of Pathology, 558 Ross Building, 720 Rutland Avenue, Baltimore, MD 21205 2196, USA
    Toxicol Pathol 39:220-33. 2011
  9. pmc The mitochondrial permeability transition pore regulates nitric oxide-mediated apoptosis of neurons induced by target deprivation
    Lee J Martin
    Department of Pathology, Division of Neuropathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci 31:359-70. 2011
  10. ncbi request reprint Transgenic mice with human mutant genes causing Parkinson's disease and amyotrophic lateral sclerosis provide common insight into mechanisms of motor neuron selective vulnerability to degeneration
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Department of Neuroscience, Johns Hopkins University School ofMedicine, Baltimore, MD 21205 2196, USA
    Rev Neurosci 18:115-36. 2007

Research Grants

  1. MECHANISMS FOR MOTOR NEURON APOPTOSIS
    Lee Martin; Fiscal Year: 2001
  2. Mechanisms of Motor Neuron Death
    Lee Martin; Fiscal Year: 2006
  3. Skeletal Muscle Mechanisms of Disease in ALS
    Lee J Martin; Fiscal Year: 2010
  4. DNA Damage/Repair and Cell Death
    Lee Martin; Fiscal Year: 2009
  5. MECHANISMS FOR MOTOR NEURON APOPTOSIS
    Lee Martin; Fiscal Year: 1999
  6. Mechanisms of Motor Neuron Death
    Lee Martin; Fiscal Year: 2005
  7. MECHANISMS OF NEURONAL APOPTOSIS IN VIVO
    Lee Martin; Fiscal Year: 2005
  8. DNA Damage/Repair and Cell Death
    Lee Martin; Fiscal Year: 2006
  9. MECHANISMS OF NEURONAL APOPTOSIS IN VIVO
    Lee Martin; Fiscal Year: 2001
  10. DNA Damage/Repair and Cell Death
    Lee Martin; Fiscal Year: 2005

Collaborators

Detail Information

Publications55

  1. pmc The olfactory bulb in newborn piglet is a reservoir of neural stem and progenitor cells
    Lee J Martin
    Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America Pathobiology Graduate Program, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America The Solomon Snyder Department of Neuroscience Graduate Program, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
    PLoS ONE 8:e81105. 2013
    ..We conclude that the piglet OB-SVZ is a reservoir of NSCs and NPCs suitable to use in autologous cell therapy in preclinical models of neonatal/pediatric brain injury. ..
  2. doi request reprint The mitochondrial permeability transition pore regulates Parkinson's disease development in mutant α-synuclein transgenic mice
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA Pathobiology Graduate Program, Johns Hopkins University School of Medicine, Baltimore, MD, USA Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA Electronic address
    Neurobiol Aging 35:1132-52. 2014
    ..Thus, mutant αSyn transgenic mice on a C57BL/6 background develop PD-like phenotypes, and the mPTP is involved in their disease mechanisms. ..
  3. pmc Aberrant regulation of DNA methylation in amyotrophic lateral sclerosis: a new target of disease mechanisms
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, 558 Ross Building, 720 Rutland Avenue, Baltimore, MD, 21205 2196, USA
    Neurotherapeutics 10:722-33. 2013
    ..Aberrant DNA methylation in vulnerable cells is a new direction for discovering mechanisms of ALS pathogenesis that could be relevant to new disease target identification and therapies for ALS. ..
  4. pmc Nuclear localization of human SOD1 and mutant SOD1-specific disruption of survival motor neuron protein complex in transgenic amyotrophic lateral sclerosis mice
    Barry Gertz
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neuropathol Exp Neurol 71:162-77. 2012
    ....
  5. ncbi request reprint Adult olfactory bulb neural precursor cell grafts provide temporary protection from motor neuron degeneration, improve motor function, and extend survival in amyotrophic lateral sclerosis mice
    Lee J Martin
    Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neuropathol Exp Neurol 66:1002-18. 2007
    ..OB-NPCs also differentiated into oligodendrocytes and astrocytes that contacted neuronal processes. We conclude that transplantation of adult OB-NPCs is therapeutic for mouse amyotrophic lateral sclerosis...
  6. pmc Generation and characterization of transgenic mice expressing mitochondrial targeted red fluorescent protein selectively in neurons: modeling mitochondriopathy in excitotoxicity and amyotrophic lateral sclerosis
    Yi Wang
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, MD 21205, USA
    Mol Neurodegener 6:75. 2011
    ....
  7. pmc Olesoxime, a cholesterol-like neuroprotectant for the potential treatment of amyotrophic lateral sclerosis
    Lee J Martin
    Johns Hopkins University School of Medicine, Departments of Pathology and Neuroscience, Baltimore, MD 21205 2196, USA
    IDrugs 13:568-80. 2010
    ..It has been granted orphan drug status for the treatment of ALS in the US and for the treatment of spinal muscular atrophy in the EU. Phase II/III clinical trials are in progress in Europe...
  8. pmc An approach to experimental synaptic pathology using green fluorescent protein-transgenic mice and gene knockout mice to show mitochondrial permeability transition pore-driven excitotoxicity in interneurons and motoneurons
    Lee J Martin
    Department of Pathology, 558 Ross Building, 720 Rutland Avenue, Baltimore, MD 21205 2196, USA
    Toxicol Pathol 39:220-33. 2011
    ....
  9. pmc The mitochondrial permeability transition pore regulates nitric oxide-mediated apoptosis of neurons induced by target deprivation
    Lee J Martin
    Department of Pathology, Division of Neuropathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci 31:359-70. 2011
    ..Our results demonstrate in adult mouse brain neurons that the mPTP functions to enhance ROS production and the mPTP and NO trigger apoptosis; thus, the mPTP is a target for neuroprotection in vivo...
  10. ncbi request reprint Transgenic mice with human mutant genes causing Parkinson's disease and amyotrophic lateral sclerosis provide common insight into mechanisms of motor neuron selective vulnerability to degeneration
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Department of Neuroscience, Johns Hopkins University School ofMedicine, Baltimore, MD 21205 2196, USA
    Rev Neurosci 18:115-36. 2007
    ..These experiments reveal that mitochondrial nitrative stress and perturbations in mitochondrial trafficking may be antecedents of neuronal cell death in animal models of PD and ALS...
  11. ncbi request reprint Mitochondriopathy in Parkinson disease and amyotrophic lateral sclerosis
    Lee J Martin
    Department of Pathology, Division of Neuropathology and Neuroscience, Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD, USA
    J Neuropathol Exp Neurol 65:1103-10. 2006
    ..This review presents how malfunctioning mitochondria might contribute to neuronal death in PD and ALS...
  12. pmc DNA damage and repair: relevance to mechanisms of neurodegeneration
    Lee J Martin
    Department of Pathology, Division of Neuropathology, and Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neuropathol Exp Neurol 67:377-87. 2008
    ..This review summarizes DNA damage and repair mechanisms and their potential relevance to the evolution of degeneration in postmitotic neurons...
  13. ncbi request reprint Mitochondrial pathobiology in ALS
    Lee J Martin
    Department of Pathology, Division of Neuropathology, and the Pathobiology Graduate Program, Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, 21205 2196, USA
    J Bioenerg Biomembr 43:569-79. 2011
    ..This paper reviews how mitochondrial pathobiology might contribute to the mechanisms of neurodegeneration in ALS...
  14. pmc The mitochondrial permeability transition pore: a molecular target for amyotrophic lateral sclerosis therapy
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    Biochim Biophys Acta 1802:186-97. 2010
    ..Thus, attention should be directed to the mPTP as a rational target for the development of drugs designed to treat ALS...
  15. pmc The mitochondrial permeability transition pore in motor neurons: involvement in the pathobiology of ALS mice
    Lee J Martin
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    Exp Neurol 218:333-46. 2009
    ..These results demonstrate that mitochondria have causal roles in the disease mechanisms in MNs in ALS mice. This work defines a new mitochondrial mechanism for MN degeneration in ALS...
  16. doi request reprint Mitochondrial pathobiology in Parkinson's disease and amyotrophic lateral sclerosis
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    J Alzheimers Dis 20:S335-56. 2010
    ..This review will present how mitochondrial pathobiology might contribute to neurodegeneration in PD and ALS and could serve as a target for drug therapy...
  17. pmc Molecular regulation of DNA damage-induced apoptosis in neurons of cerebral cortex
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205 2196, USA
    Cereb Cortex 19:1273-93. 2009
    ..This molecular network operates through variations depending on neuron maturity...
  18. pmc Inhibitory synaptic regulation of motoneurons: a new target of disease mechanisms in amyotrophic lateral sclerosis
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, 558 Ross Building, 720 Rutland Avenue, Baltimore, MD 21205 2196, USA
    Mol Neurobiol 45:30-42. 2012
    ..Abnormal synaptic inhibition resulting from dysfunction of interneurons and motoneuron GlyRs is a new direction for unveiling mechanisms of ALS pathogenesis that could be relevant to new therapies for ALS...
  19. ncbi request reprint Early events of target deprivation/axotomy-induced neuronal apoptosis in vivo: oxidative stress, DNA damage, p53 phosphorylation and subcellular redistribution of death proteins
    Lee J Martin
    Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurochem 85:234-47. 2003
    ....
  20. ncbi request reprint Parkinson's disease alpha-synuclein transgenic mice develop neuronal mitochondrial degeneration and cell death
    Lee J Martin
    Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neurosci 26:41-50. 2006
    ..Thus, A53T mutant mice develop intraneuronal inclusions, mitochondrial DNA damage and degeneration, and apoptotic-like death of neocortical, brainstem, and motor neurons...
  21. ncbi request reprint Motor neuron degeneration in amyotrophic lateral sclerosis mutant superoxide dismutase-1 transgenic mice: mechanisms of mitochondriopathy and cell death
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Comp Neurol 500:20-46. 2007
    ..The data support roles for oxidative stress, protein nitration and aggregation, and excitotoxicity as participants in the process of MN degeneration caused by mSOD1...
  22. pmc Dopamine receptor modulation of hypoxic-ischemic neuronal injury in striatum of newborn piglets
    Zeng Jin Yang
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    J Cereb Blood Flow Metab 27:1339-51. 2007
    ..Furthermore, mechanisms of D1 receptor toxicity may involve DARPP-32-dependent phosphorylation of NMDA receptor NR1 and Na(+),K(+)-ATPase...
  23. pmc Rapid NMDA receptor phosphorylation and oxidative stress precede striatal neurodegeneration after hypoxic ischemia in newborn piglets and are attenuated with hypothermia
    Dawn Mueller-Burke
    School of Nursing, University of Maryland at Baltimore, Baltimore, MD 21201, USA
    Int J Dev Neurosci 26:67-76. 2008
    ..Postasphyxic, mild whole body hypothermia provides neuroprotection by suppressing N-methyl-d-aspartate receptor phosphorylation and protein oxidation...
  24. pmc Inducible nitric oxide synthase is present in motor neuron mitochondria and Schwann cells and contributes to disease mechanisms in ALS mice
    Kevin Chen
    Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine, 558 Ross Building, 720 Rutland Avenue, Baltimore, MA 21205 2196, USA
    Brain Struct Funct 214:219-34. 2010
    ..This work identifies two new potential early mechanisms for MN degeneration in mouse ALS involving iNOS at MN mitochondria and Schwann cells and suggests that therapies targeting iNOS might be beneficial in treating human ALS...
  25. ncbi request reprint Altered expression and phosphorylation of N-methyl-D-aspartate receptors in piglet striatum after hypoxia-ischemia
    Anne Marie Guerguerian
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Brain Res Mol Brain Res 104:66-80. 2002
    ....
  26. ncbi request reprint Rapid subcellular redistribution of Bax precedes caspase-3 and endonuclease activation during excitotoxic neuronal apoptosis in rat brain
    Josephine Lok
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neurotrauma 19:815-28. 2002
    ....
  27. ncbi request reprint The adult neural stem and progenitor cell niche is altered in amyotrophic lateral sclerosis mouse brain
    Zhiping Liu
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Comp Neurol 497:468-88. 2006
    ..We conclude that adult mSOD1 ALS mice have abnormalities in forebrain NSCs, but the essential features of NSC/NPCs remained in presymptomatic and symptomatic mice...
  28. doi request reprint Motor neuron disease occurring in a mutant dynactin mouse model is characterized by defects in vesicular trafficking
    Fiona M Laird
    Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci 28:1997-2005. 2008
    ..This novel mouse model will be instrumental for not only clarifying disease mechanisms in ALS, but also for testing therapeutic strategies to ameliorate this devastating disease...
  29. ncbi request reprint Transplanted human embryonic germ cell-derived neural stem cells replace neurons and oligodendrocytes in the forebrain of neonatal mice with excitotoxic brain damage
    Dawn Mueller
    Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    J Neurosci Res 82:592-608. 2005
    ..c) 2005 Wiley-Liss, Inc...
  30. pmc Skeletal muscle-restricted expression of human SOD1 causes motor neuron degeneration in transgenic mice
    Margaret Wong
    Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine, 558 Ross Building, 720 Rutland Avenue, Baltimore, MD 21205 2196, USA
    Hum Mol Genet 19:2284-302. 2010
    ..The discovery of instigating molecular toxicities or disease progression determinants within skeletal muscle could be very valuable for the development of new effective therapies for the treatment and cure of ALS...
  31. ncbi request reprint Long-term culture of mouse cortical neurons as a model for neuronal development, aging, and death
    Christian Lesuisse
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurobiol 51:9-23. 2002
    ..These neurons sustain protein nitration during aging and exhibit age-related variations in the biochemistry of neuronal apoptosis...
  32. ncbi request reprint DNA base-excision repair enzyme apurinic/apyrimidinic endonuclease/redox factor-1 is increased and competent in the brain and spinal cord of individuals with amyotrophic lateral sclerosis
    Arif Y Shaikh
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205 2196, USA
    Neuromolecular Med 2:47-60. 2002
    ..We conclude that mechanisms for DNA repair are activated in ALS, supporting the possibility that DNA damage is an upstream mechanism for motor neuron degeneration in this disease...
  33. ncbi request reprint Immature and mature cortical neurons engage different apoptotic mechanisms involving caspase-3 and the mitogen-activated protein kinase pathway
    Christian Lesuisse
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Cereb Blood Flow Metab 22:935-50. 2002
    ..The results show that immature and mature cortical neurons engage different signaling mechanisms in MAP kinase and caspase pathways during apoptosis; thus, neuron age influences the mechanisms and progression of apoptosis...
  34. ncbi request reprint Neonatal mice lacking functional Fas death receptors are resistant to hypoxic-ischemic brain injury
    Ernest M Graham
    Department of Gyn Ob, Division of Maternal Fetal Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Neurobiol Dis 17:89-98. 2004
    ..Basal levels of endogenous decoy proteins may modulate the response to Fas death receptor signaling and provide a novel approach to understanding mechanisms of neonatal brain injury...
  35. ncbi request reprint Axonal transection in adult rat brain induces transsynaptic apoptosis and persistent atrophy of target neurons
    Stephen D Ginsberg
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neurotrauma 19:99-109. 2002
    ..This transneuronal degeneration can be classified as sustained neuronal atrophy or transsynaptic apoptosis...
  36. ncbi request reprint Pluripotent fates and tissue regenerative potential of adult olfactory bulb neural stem and progenitor cells
    Zhiping Liu
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neurotrauma 21:1479-99. 2004
    ....
  37. pmc Synphilin-1 attenuates neuronal degeneration in the A53T alpha-synuclein transgenic mouse model
    Wanli W Smith
    Division of Neurobiology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Hum Mol Genet 19:2087-98. 2010
    ..These studies demonstrate that synphilin-1 can diminish the severity of alpha-synucleinopathy and play a neuroprotective role against A53T alpha-synuclein toxicity in vivo...
  38. ncbi request reprint Neuronal cell death in neonatal hypoxia-ischemia
    Frances J Northington
    Division of Neonatology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Ann Neurol 69:743-58. 2011
    ..The accurate identification of the various cell death chreodes and their mechanisms unfolding within the immature brain matrix could provide fresh insight for developing meaningful therapies for neonatal and pediatric HIE...
  39. pmc Sigma receptor ligand 4-phenyl-1-(4-phenylbutyl)-piperidine modulates neuronal nitric oxide synthase/postsynaptic density-95 coupling mechanisms and protects against neonatal ischemic degeneration of striatal neurons
    Zeng Jin Yang
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, MD 21205, USA
    Exp Neurol 221:166-74. 2010
    ..These findings indicate that PPBP protects striatal neurons in a large animal model of neonatal H-I and that the protection is associated with decreased coupling of nNOS to PSD-95...
  40. ncbi request reprint DNA damage profiling in motor neurons: a single-cell analysis by comet assay
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Neurochem Res 27:1093-104. 2002
    ..Viable mature MN can be isolated and used for in vitro models of MN genotoxicity and can be isolated from in vivo models of MN degeneration for profiling DNA damage on a single-cell basis...
  41. ncbi request reprint Hypothermia for 24 hours after asphyxic cardiac arrest in piglets provides striatal neuroprotection that is sustained 10 days after rewarming
    Dawn M Agnew
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Hospital, Blalock 1404, 600 N Wolfe Street, Baltimore, MD 21287 U S A
    Pediatr Res 54:253-62. 2003
    ....
  42. ncbi request reprint Nitration of the striatal Na,K-ATPase alpha3 isoform occurs in normal brain development but is not increased during hypoxia-ischemia in newborn piglets
    W Christopher Golden
    Department of Pediatrics, Eudowood Neonatal Pulmonary Division, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    Neurochem Res 28:1883-9. 2003
    ..Protein nitration may serve as marker of other normal, noninjurious cell processes in the developing brain...
  43. ncbi request reprint Injury-induced spinal motor neuron apoptosis is preceded by DNA single-strand breaks and is p53- and Bax-dependent
    Lee J Martin
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurobiol 50:181-97. 2002
    ..We conclude that adult motor neuron death after nerve avulsion is DNA damage-induced, p53- and Bax-dependent apoptosis...
  44. ncbi request reprint Apoptosis in perinatal hypoxic-ischemic brain injury: how important is it and should it be inhibited?
    Frances J Northington
    Department of Pediatrics, Eudowood Neonatal Pulmonary Division, Dept of Pediatrics, CMSC 6 104, Johns Hopkins University School of Medicine, 600 N Wolfe St, Baltimore, MD 21287, USA
    Brain Res Brain Res Rev 50:244-57. 2005
    ..This review summarizes current evidence for apoptotic mechanisms in perinatal brain injury and addresses issues pertinent to the development of antiapoptosis therapies for perinatal HI and stroke...
  45. ncbi request reprint Adult motor neuron apoptosis is mediated by nitric oxide and Fas death receptor linked by DNA damage and p53 activation
    Lee J Martin
    Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Neurosci 25:6449-59. 2005
    ..Thus, adult spinal MN apoptosis is mediated by upstream NO and ONOO- genotoxicity and downstream p53 and Fas activation and is shifted to necrosis by mutant SOD1...
  46. pmc Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI
    Frances J Northington
    Neonatal Research Laboratory, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    J Cereb Blood Flow Metab 31:178-89. 2011
    ..The effects of necrostatin treatment after HI reflect the importance of necrosis in the delayed phases of neonatal brain injury and represent a new direction for therapy of neonatal HI...
  47. pmc Glycinergic innervation of motoneurons is deficient in amyotrophic lateral sclerosis mice: a quantitative confocal analysis
    Qing Chang
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Am J Pathol 174:574-85. 2009
    ..Thus, either the selective loss of inhibitory glycinergic regulation of motoneuron function or glycinergic interneuron degeneration contributes to motoneuron degeneration in amyotrophic lateral sclerosis...
  48. ncbi request reprint Histopathological and behavioral characterization of a novel model of cardiac arrest and cardiopulmonary resuscitation in mice
    Julia Kofler
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, 720 Rutland Avenue, Baltimore, MD 21205, USA
    J Neurosci Methods 136:33-44. 2004
    ..A dissociation between functional and histological outcome was found emphasizing the importance of combining both outcome measures for evaluation of neuroprotective strategies...
  49. pmc Delayed neural network degeneration after neonatal hypoxia-ischemia
    Brian S Stone
    Department of Pediatrics, Eudowood Neonatal Pulmonary Division, Neonatal Research Laboratory, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Ann Neurol 64:535-46. 2008
    ....
  50. ncbi request reprint Olfactory bulb core is a rich source of neural progenitor and stem cells in adult rodent and human
    Zhiping Liu
    Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Comp Neurol 459:368-91. 2003
    ..Cocultured OB-derived neural stem cells with myoblast cells also generated nonneural cell progeny. We conclude that the adult mammalian OB core is a reservoir of neural progenitor cells and pluripotent neural stem cells...
  51. ncbi request reprint In situ immunoradiographic method for quantification of specific proteins in normal and ischemic brain regions
    Annette Rebel
    Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    J Neurosci Methods 143:227-35. 2005
    ..The disadvantage of the falsely positive overestimation of protein immunoreactivity after stroke with the immunoperoxidase method has to be weighted with the advantage of the cellular resolution...
  52. pmc Resistance to Alzheimer's pathology is associated with nuclear hypertrophy in neurons
    Miguel Angel Riudavets
    Division of Neuropathology, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Neurobiol Aging 28:1484-92. 2007
    ..This nuclear hypertrophy may represent an early neuronal reaction to Abeta or Tau, or a compensatory mechanism which forestalls the progression of AD and allows the brain to resist the development of dementia...
  53. pmc Neuropathologic studies of the Baltimore Longitudinal Study of Aging (BLSA)
    RICHARD J O'BRIEN
    Department of Neurology, School of Medicine, Johns Hopkins University, Baltimore, MD 21224, USA
    J Alzheimers Dis 18:665-75. 2009
    ..e., neuronal hypertrophy and synaptic plasticity) whereas a failure of compensation may culminate in disease...
  54. pmc Amyotrophic lateral sclerosis 2-deficiency leads to neuronal degeneration in amyotrophic lateral sclerosis through altered AMPA receptor trafficking
    Chen Lai
    Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892 3707, USA
    J Neurosci 26:11798-806. 2006
    ....

Research Grants25

  1. MECHANISMS FOR MOTOR NEURON APOPTOSIS
    Lee Martin; Fiscal Year: 2001
    ..These studies should lead to a better understanding of motor neuron death and to the design of new therapeutic experiments critical for the future treatment of ALS. ..
  2. Mechanisms of Motor Neuron Death
    Lee Martin; Fiscal Year: 2006
    ..abstract_text> ..
  3. Skeletal Muscle Mechanisms of Disease in ALS
    Lee J Martin; Fiscal Year: 2010
    ..This work will determine if abnormalities in skeletal muscle have causal roles in the disease mechanisms. Skeletal muscle could provide new tissue- and molecular targets for drug discovery in ALS. ..
  4. DNA Damage/Repair and Cell Death
    Lee Martin; Fiscal Year: 2009
    ....
  5. MECHANISMS FOR MOTOR NEURON APOPTOSIS
    Lee Martin; Fiscal Year: 1999
    ..These studies should lead to a better understanding of motor neuron death and to the design of new therapeutic experiments critical for the future treatment of ALS. ..
  6. Mechanisms of Motor Neuron Death
    Lee Martin; Fiscal Year: 2005
    ..abstract_text> ..
  7. MECHANISMS OF NEURONAL APOPTOSIS IN VIVO
    Lee Martin; Fiscal Year: 2005
    ..This work can define a new mitochondrial mechanism for target deprivation-induced neurodegeneration and can improve the understanding of the cellular and molecular mechanisms of neuronal apoptosis in vivo ..
  8. DNA Damage/Repair and Cell Death
    Lee Martin; Fiscal Year: 2006
    ....
  9. MECHANISMS OF NEURONAL APOPTOSIS IN VIVO
    Lee Martin; Fiscal Year: 2001
    ..These studies will identify possible molecular mechanisms of neuronal apoptosis in vivo and could lead to the design of new therapeutic neuroprotection experiments critical for the future treatment of AD and ALS. ..
  10. DNA Damage/Repair and Cell Death
    Lee Martin; Fiscal Year: 2005
    ....
  11. DNA Damage/Repair and Cell Death
    Lee Martin; Fiscal Year: 2007
    ....
  12. Mechanisms of Motor Neuron Death
    Lee Martin; Fiscal Year: 2004
    ..abstract_text> ..
  13. MECHANISMS OF NEURONAL APOPTOSIS IN VIVO
    Lee Martin; Fiscal Year: 2003
    ..These studies will identify possible molecular mechanisms of neuronal apoptosis in vivo and could lead to the design of new therapeutic neuroprotection experiments critical for the future treatment of AD and ALS. ..
  14. MECHANISMS OF NEURONAL APOPTOSIS IN VIVO
    Lee Martin; Fiscal Year: 2007
    ..This work can define a new mitochondrial mechanism for target deprivation-induced neurodegeneration and can improve the understanding of the cellular and molecular mechanisms of neuronal apoptosis in vivo ..
  15. MECHANISMS OF NEURONAL APOPTOSIS IN VIVO
    Lee Martin; Fiscal Year: 2002
    ..These studies will identify possible molecular mechanisms of neuronal apoptosis in vivo and could lead to the design of new therapeutic neuroprotection experiments critical for the future treatment of AD and ALS. ..
  16. Mechanisms of Motor Neuron Death
    Lee Martin; Fiscal Year: 2003
    ..abstract_text> ..
  17. MECHANISMS OF NEURONAL APOPTOSIS IN VIVO
    Lee Martin; Fiscal Year: 2006
    ..This work can define a new mitochondrial mechanism for target deprivation-induced neurodegeneration and can improve the understanding of the cellular and molecular mechanisms of neuronal apoptosis in vivo ..
  18. MECHANISMS FOR MOTOR NEURON APOPTOSIS
    Lee Martin; Fiscal Year: 2000
    ..These studies should lead to a better understanding of motor neuron death and to the design of new therapeutic experiments critical for the future treatment of ALS. ..
  19. MECHANISMS OF NEURONAL APOPTOSIS IN VIVO
    Lee Martin; Fiscal Year: 2009
    ..This work can define a new mitochondrial mechanism for target deprivation-induced neurodegeneration and can improve the understanding of the cellular and molecular mechanisms of neuronal apoptosis in vivo ..