Ted Dawson

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. pmc Conditional transgenic mice expressing C-terminally truncated human alpha-synuclein (alphaSyn119) exhibit reduced striatal dopamine without loss of nigrostriatal pathway dopaminergic neurons
    João Paulo L Daher
    Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, USA
    Mol Neurodegener 4:34. 2009
  2. pmc Dynamic and redundant regulation of LRRK2 and LRRK1 expression
    Saskia Biskup
    Institute for Cell Engineering and Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, USA
    BMC Neurosci 8:102. 2007
  3. doi request reprint A lysosomal lair for a pathogenic protein pair
    Ted M Dawson
    Neuroregeneration Program, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Sci Transl Med 3:91ps28. 2011
  4. ncbi request reprint New animal models for Parkinson's disease
    T M Dawson
    Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    Cell 101:115-8. 2000
  5. doi request reprint Unraveling the role of defective genes in Parkinson's disease
    Ted M Dawson
    Institute for Cell Engineering, Departments of Neurology and Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Parkinsonism Relat Disord 13:S248-9. 2007
  6. pmc Rare genetic mutations shed light on the pathogenesis of Parkinson disease
    Ted M Dawson
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    J Clin Invest 111:145-51. 2003
  7. ncbi request reprint Molecular pathways of neurodegeneration in Parkinson's disease
    Ted M Dawson
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Science 302:819-22. 2003
  8. ncbi request reprint Neuroprotective and neurorestorative strategies for Parkinson's disease
    Ted M Dawson
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    Nat Neurosci 5:1058-61. 2002
  9. doi request reprint Understanding microRNAs in neurodegeneration
    Stephen M Eacker
    Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Nat Rev Neurosci 10:837-41. 2009
  10. ncbi request reprint Preconditioning-mediated neuroprotection through erythropoietin?
    Ted M Dawson
    Institute for Cellular Engineering, Department of Neurology and Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Lancet 359:96-7. 2002

Collaborators

Detail Information

Publications68

  1. pmc Conditional transgenic mice expressing C-terminally truncated human alpha-synuclein (alphaSyn119) exhibit reduced striatal dopamine without loss of nigrostriatal pathway dopaminergic neurons
    João Paulo L Daher
    Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, USA
    Mol Neurodegener 4:34. 2009
    ..abstract:..
  2. pmc Dynamic and redundant regulation of LRRK2 and LRRK1 expression
    Saskia Biskup
    Institute for Cell Engineering and Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, USA
    BMC Neurosci 8:102. 2007
    ..The expression profiles of the murine LRRK proteins have not been fully described and insufficiently characterized antibodies have produced conflicting results in the literature...
  3. doi request reprint A lysosomal lair for a pathogenic protein pair
    Ted M Dawson
    Neuroregeneration Program, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Sci Transl Med 3:91ps28. 2011
    ..Understanding how lysosomes are implicated in PD may reveal new therapeutic targets for treating this disease...
  4. ncbi request reprint New animal models for Parkinson's disease
    T M Dawson
    Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    Cell 101:115-8. 2000
  5. doi request reprint Unraveling the role of defective genes in Parkinson's disease
    Ted M Dawson
    Institute for Cell Engineering, Departments of Neurology and Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Parkinsonism Relat Disord 13:S248-9. 2007
    ..Here I shortly review the major genes implicated in autosomal dominant and autosomal recessive PD. Understanding how mutations in these PD associated genes holds particular promise for development of new therapies to treat PD...
  6. pmc Rare genetic mutations shed light on the pathogenesis of Parkinson disease
    Ted M Dawson
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    J Clin Invest 111:145-51. 2003
  7. ncbi request reprint Molecular pathways of neurodegeneration in Parkinson's disease
    Ted M Dawson
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Science 302:819-22. 2003
    ..Strategies aimed at restoring complex I activity, reducing oxidative stress and alpha-synuclein aggregation, and enhancing protein degradation may hold particular promise as powerful neuroprotective agents in the treatment of PD...
  8. ncbi request reprint Neuroprotective and neurorestorative strategies for Parkinson's disease
    Ted M Dawson
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    Nat Neurosci 5:1058-61. 2002
    ..Here we review many of these advances, highlighting areas and strategies that might be particularly suited to the development of innovative approaches that prevent degeneration and/or restore function in Parkinson's disease...
  9. doi request reprint Understanding microRNAs in neurodegeneration
    Stephen M Eacker
    Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Nat Rev Neurosci 10:837-41. 2009
    ....
  10. ncbi request reprint Preconditioning-mediated neuroprotection through erythropoietin?
    Ted M Dawson
    Institute for Cellular Engineering, Department of Neurology and Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Lancet 359:96-7. 2002
  11. pmc Genetic animal models of Parkinson's disease
    Ted M Dawson
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Neuron 66:646-61. 2010
    ..In this review, we discuss the animal models for these genetic causes of PD, their limitations, and value. Moreover, we discuss future directions and potential strategies for optimization of the genetic models...
  12. ncbi request reprint Animal models of PD: pieces of the same puzzle?
    Ted Dawson
    The Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Neuron 35:219-22. 2002
    ..This has prompted us to critically review the current animal models for PD and discuss how these models may yield fresh insights into the pathogenesis of PD, as well as new therapeutic opportunities...
  13. doi request reprint The role of parkin in familial and sporadic Parkinson's disease
    Ted M Dawson
    Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Mov Disord 25:S32-9. 2010
    ..Loss of parkin's E3 ligase activity is thought to play a pathogenic role in both inherited and sporadic PD. Here, we review parkin biology and pathobiology and its role in the pathogenesis of PD...
  14. ncbi request reprint Value of genetic models in understanding the cause and mechanisms of Parkinson's disease
    Darren J Moore
    Institute for Cell Engineering and Department of Neurology, Johns Hopkins University School of Medicine, 733 North Broadway, Broadway Research Building, Suite 711, Baltimore, MD 21205, USA
    Curr Neurol Neurosci Rep 8:288-96. 2008
    ..In this article, we discuss these mammalian genetic models of PD and what they have revealed about the cause and mechanisms of this disease...
  15. ncbi request reprint Kinase activity of mutant LRRK2 mediates neuronal toxicity
    Wanli W Smith
    Department of Psychiatry, Division of Neurobiology, Johns Hopkins University School of Medicine, CMSC 8 121, 600 North Wolfe Street, Baltimore, Maryland 21287, USA
    Nat Neurosci 9:1231-3. 2006
    ..These data elucidate the pathogenesis of LRRK2-linked Parkinson disease, potentially illuminate mechanisms of sporadic Parkinson disease and suggest therapeutic targets...
  16. pmc Diagnosis and treatment of Parkinson disease: molecules to medicine
    Joseph M Savitt
    Institute for Cell Engineering, Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Clin Invest 116:1744-54. 2006
    ....
  17. ncbi request reprint Parkin blushed by PINK1
    Jeanne M M Tan
    Institute for Cell Engineering, Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Neuron 50:527-9. 2006
    ..Thus, PINK1 and parkin appear to function in a common pathway suggesting a convergence of the two genes most commonly associated with autosomal recessive PD...
  18. ncbi request reprint Inclusion body formation and neurodegeneration are parkin independent in a mouse model of alpha-synucleinopathy
    Rainer von Coelln
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci 26:3685-96. 2006
    ....
  19. pmc Neuroprotection by pharmacologic blockade of the GAPDH death cascade
    Makoto R Hara
    Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 103:3887-9. 2006
    ..In mice treated with the dopamine neuronal toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), low doses of deprenyl prevent binding of GAPDH and Siah1 in the dopamine-enriched corpus striatum...
  20. ncbi request reprint Lessons from Drosophila models of DJ-1 deficiency
    Darren J Moore
    Institute for Cell Engineering, Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Sci Aging Knowledge Environ 2006:pe2. 2006
    ..DJ-1-deficient fly models further highlight the utility of Drosophila as an important tool for elucidating protein function and for modeling neurodegenerative disease...
  21. pmc Leucine-rich repeat kinase 2 (LRRK2) interacts with parkin, and mutant LRRK2 induces neuronal degeneration
    Wanli W Smith
    Department of Psychiatry, Division of Neurobiology, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Proc Natl Acad Sci U S A 102:18676-81. 2005
    ....
  22. ncbi request reprint Stress-induced alterations in parkin solubility promote parkin aggregation and compromise parkin's protective function
    Cheng Wang
    Neurodegeneration Research Laboratory, National Neuroscience Institute, Singapore
    Hum Mol Genet 14:3885-97. 2005
    ..Mechanistically, our results provide a link between the influence of environmental and intrinsic factors and genetic susceptibilities in PD pathogenesis...
  23. ncbi request reprint Endoplasmic reticulum stress and mitochondrial cell death pathways mediate A53T mutant alpha-synuclein-induced toxicity
    Wanli W Smith
    Department of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Hum Mol Genet 14:3801-11. 2005
    ..This study sheds light into the pathogenesis of alpha-synuclein cellular toxicity in PD and provides a cell model for screening PD therapeutic agents...
  24. ncbi request reprint Parkin-mediated lysine 63-linked polyubiquitination: a link to protein inclusions formation in Parkinson's and other conformational diseases?
    Kah Leong Lim
    Neurodegeneration Research Laboratory, National Neuroscience Institute, Singapore
    Neurobiol Aging 27:524-9. 2006
    ..Mechanistically, the involvement of a "non-degradative" mode of ubiquitination in protein inclusion formation is an attractive explanation for how proteins are seemingly stabilized within inclusions...
  25. ncbi request reprint Expression and localization of Parkinson's disease-associated leucine-rich repeat kinase 2 in the mouse brain
    Shinji Higashi
    Laboratory of Molecular Neuroscience, The Babraham Institute, Babraham, Cambridge, UK
    J Neurochem 100:368-81. 2007
    ....
  26. ncbi request reprint Parkinson's disease-associated mutations in LRRK2 link enhanced GTP-binding and kinase activities to neuronal toxicity
    Andrew B West
    Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Hum Mol Genet 16:223-32. 2007
    ..These results suggest a link between LRRK2 kinase activity and pathogenic mechanisms relating to neurodegeneration, further supporting a gain-of-function role for LRRK2 mutations...
  27. doi request reprint Non-autonomous cell death in Parkinson's disease
    Ted M Dawson
    Lancet Neurol 7:474-5. 2008
  28. pmc The chaperone activity of heat shock protein 90 is critical for maintaining the stability of leucine-rich repeat kinase 2
    Lizhen Wang
    Unit of Transgenesis, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, Maryland 20892, USA
    J Neurosci 28:3384-91. 2008
    ..Therefore, inhibition of LRRK2 kinase activity can be achieved by blocking Hsp90-mediated chaperone activity and Hsp90 inhibitors may serve as potential anti-PD drugs...
  29. doi request reprint Role of tuberin in neuronal degeneration
    Samy L Habib
    Department of Medicine, University of Texas Health Science Center, San Antonio, TX, USA
    Neurochem Res 33:1113-6. 2008
    ..Our data provide new information regarding the possible role of tuberin dysfunction in major neurodegenerative disorders, such as AD and PD, whereby inhibition of tuberin function may trigger an onset of neuronal cell death...
  30. pmc Morphometry of the human substantia nigra in ageing and Parkinson's disease
    Gay Rudow
    Neuropathology, Johns Hopkins School of Medicine, Ross Research Building 555, 720 Rutland Avenue, Baltimore, MD 21205, USA
    Acta Neuropathol 115:461-70. 2008
    ..Presumably, this compensatory mechanism breaks down or is overwhelmed by the pathological events of PD leading to the onset of the characteristic motor disturbances...
  31. doi request reprint Parkin mediates the degradation-independent ubiquitination of Hsp70
    Darren J Moore
    Institute for Cell Engineering, and Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurochem 105:1806-19. 2008
    ....
  32. pmc MPTP and DSP-4 susceptibility of substantia nigra and locus coeruleus catecholaminergic neurons in mice is independent of parkin activity
    Bobby Thomas
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Neurobiol Dis 26:312-22. 2007
    ..These findings suggest that absence of parkin in mice does not increase susceptibility to the loss of catecholaminergic neurons upon exposure to both dopaminergic and noradrenergic neurotoxins...
  33. ncbi request reprint Lysine 63-linked ubiquitination promotes the formation and autophagic clearance of protein inclusions associated with neurodegenerative diseases
    Jeanne M M Tan
    Neurodegeneration Research Lab, National Neuroscience Institute, Singapore, Singapore
    Hum Mol Genet 17:431-9. 2008
    ..Collectively, our results provide a novel mechanistic route that underlies the life cycle of an inclusion body. Harnessing this pathway may offer innovative approaches in the treatment of neurodegenerative disorders...
  34. pmc DJ-1 gene deletion reveals that DJ-1 is an atypical peroxiredoxin-like peroxidase
    Eva Andres-Mateos
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, 733 North Broadway, Suite 731, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 104:14807-12. 2007
    ..Taken together these data indicate that the DJ-1 KO mice have a deficit in scavenging mitochondrial H(2)O(2) due to the physiological function of DJ-1 as an atypical peroxiredoxin-like peroxidase...
  35. ncbi request reprint Localization of Parkinson's disease-associated LRRK2 in normal and pathological human brain
    Shinji Higashi
    Laboratory of Molecular Neuroscience, The Babraham Institute, Babraham, Cambridge, UK
    Brain Res 1155:208-19. 2007
    ..The localization of LRRK2 to key neuronal populations throughout the nigrostriatal dopaminergic pathway is consistent with the involvement of LRRK2 in the molecular pathogenesis of familial and sporadic parkinsonism...
  36. ncbi request reprint Relative sensitivity of parkin and other cysteine-containing enzymes to stress-induced solubility alterations
    Esther S P Wong
    Neurodegeneration Research Laboratory and Parkinson s Disease and Movement Disorders Center, National Neuroscience Institute, Singapore 308433
    J Biol Chem 282:12310-8. 2007
    ..However, parkin appears to be uniquely sensitive to DA-mediated stress, the specificity of which is likely due to DA modification of 2 Cys residues on parkin (Cys-268 and Cys-323) that are distinct from other RING-IBR-RING members...
  37. ncbi request reprint Neurotoxicity and behavioral deficits associated with Septin 5 accumulation in dopaminergic neurons
    Jin H Son
    Laboratory of Molecular Neurobiology, The W M Burke Medical Research Institute, White Plains, New York 10605, USA
    J Neurochem 94:1040-53. 2005
    ..These data suggest that a threshold level of Septin 5 accumulation is required for DAergic cell loss and that l-DOPA-responsive motor deficits can occur even in the presence of elevated DA...
  38. ncbi request reprint Familial-associated mutations differentially disrupt the solubility, localization, binding and ubiquitination properties of parkin
    Sathya R Sriram
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Hum Mol Genet 14:2571-86. 2005
    ....
  39. ncbi request reprint A missense mutation (L166P) in DJ-1, linked to familial Parkinson's disease, confers reduced protein stability and impairs homo-oligomerization
    Darren J Moore
    Institute for Cell Engineering, Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurochem 87:1558-67. 2003
    ..These properties of the L166P mutation may contribute to the loss of normal DJ-1 function and are likely to be the underlying cause of early onset PD in affected members of the Italian kindred...
  40. ncbi request reprint Poly(ADP-ribose) polymerase-1 and apoptosis inducing factor in neurotoxicity
    Seong Woon Yu
    Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Neurobiol Dis 14:303-17. 2003
    ..These recent findings suggest that AIF maybe a target for development of future therapeutic treatment for many neurological disorders involving excitotoxicity...
  41. ncbi request reprint Caught in the act: alpha-synuclein is the culprit in Parkinson's disease
    Jason L Eriksen
    Department of Neurogenetics, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224, USA
    Neuron 40:453-6. 2003
    ..This review discusses how insights gained from these studies of alpha-synuclein may direct future research into Parkinson's disease...
  42. ncbi request reprint Nuclear localization of a non-caspase truncation product of atrophin-1, with an expanded polyglutamine repeat, increases cellular toxicity
    Frederick C Nucifora
    Division of Neurobiology, Department of Psychiatry, and The Program in Cellular and Molecular Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 2196, USA
    J Biol Chem 278:13047-55. 2003
    ..These data indicate that truncation of atrophin-1 may alter its ability to shuttle between the nucleus and cytoplasm, leading to abnormal nuclear interactions and cell toxicity...
  43. ncbi request reprint New insights into Parkinson's disease
    Kenny K K Chung
    Institute for Cell Engineering, Department of Neurology, Johns Hopkins University School of Medicine, 600 N Wolfe St, Carnegie 2 214, Baltimore, Maryland 21287, USA
    J Neurol 250:III15-24. 2003
    ..These important findings serve as the foundation for discovering new pathways that may lead to the development of new therapies for PD...
  44. ncbi request reprint Role for the ubiquitin-proteasome system in Parkinson's disease and other neurodegenerative brain amyloidoses
    Darren J Moore
    Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Neuromolecular Med 4:95-108. 2003
    ....
  45. ncbi request reprint Novel monoclonal antibodies demonstrate biochemical variation of brain parkin with age
    Aaron C Pawlyk
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Biol Chem 278:48120-8. 2003
    ....
  46. ncbi request reprint Apoptosis inducing factor and PARP-mediated injury in the MPTP mouse model of Parkinson's disease
    Hongmin Wang
    Department of Neurology, Neuroscience, and Physiology, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    Ann N Y Acad Sci 991:132-9. 2003
    ..This article briefly reviews the experimental findings regarding excitotoxicity, PARP activation, and AIF translocation in MPTP toxicity and dopaminergic neuronal cell death...
  47. ncbi request reprint The cast of molecular characters in Parkinson's disease: felons, conspirators, and suspects
    Kah Leong Lim
    Neurodegeneration Research Laboratory, National Neuroscience Institute, 11 Jalan Tan Tock Seng, Singapore 308433
    Ann N Y Acad Sci 991:80-92. 2003
    ..This review discusses the role of the UPS, as well as the modus operandi of the three PD candidate felons (alpha-synuclein, parkin, and UCHL1) along with their conspirators in bringing about dopaminergic cell death in PD...
  48. ncbi request reprint BAK alters neuronal excitability and can switch from anti- to pro-death function during postnatal development
    Yihru Fannjiang
    Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Dev Cell 4:575-85. 2003
    ..BAK can alter neurotransmitter release in a direction consistent with its protective effects on neurons and mice. These findings suggest that BAK inhibits cell death by modifying neuronal excitability...
  49. ncbi request reprint The genetics of Parkinson's disease
    Kah Leong Lim
    Department of Neurology, Institute for Cell Engineering, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Carnegie 214, Baltimore, MD 21287, USA
    Curr Neurol Neurosci Rep 2:439-46. 2002
    ..Such studies undoubtedly will be instrumental in establishing the susceptibility genes involved in idiopathic PD. This article reviews the recent advances in the genetics of PD...
  50. pmc Apoptosis-inducing factor is involved in the regulation of caspase-independent neuronal cell death
    Sean P Cregan
    Ottawa Health Research Institute, Department of Neuroscience, University of Ottawa, Ontario, Canada, K1H 8M5
    J Cell Biol 158:507-17. 2002
    ..Taken together, our results suggest that AIF may be an important therapeutic target for the treatment of neuronal injury...
  51. ncbi request reprint Mediation of poly(ADP-ribose) polymerase-1-dependent cell death by apoptosis-inducing factor
    Seong Woon Yu
    Department of Neurology and Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Science 297:259-63. 2002
    ..These data support a model in which PARP-1 activation signals AIF release from mitochondria, resulting in a caspase-independent pathway of programmed cell death...
  52. ncbi request reprint CHIP and Hsp70 regulate tau ubiquitination, degradation and aggregation
    Leonard Petrucelli
    Mayo Clinic, Jacksonville, FL 32224, USA
    Hum Mol Genet 13:703-14. 2004
    ..Hsp70/CHIP may therefore play an important role in the pathogenesis of tauopathies and also represents a potential therapeutic target...
  53. ncbi request reprint What have genetically engineered mice taught us about ischemic injury?
    Dong Liang
    Department of Neurology, Johns Hopkins University School of Medicine, 733 North Broadway Street, Suit 731, Baltimore, MD 21205, USA
    Curr Mol Med 4:207-25. 2004
    ..Findings from experimental stroke studies in genetically engineered animals are discussed...
  54. ncbi request reprint S-nitrosylation of parkin regulates ubiquitination and compromises parkin's protective function
    Kenny K K Chung
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Science 304:1328-31. 2004
    ..The inhibition of parkin's ubiquitin E3 ligase activity by S-nitrosylation could contribute to the degenerative process in these disorders by impairing the ubiquitination of parkin substrates...
  55. ncbi request reprint Molecular pathophysiology of Parkinson's disease
    Darren J Moore
    Institute for Cell Engineering, Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Annu Rev Neurosci 28:57-87. 2005
    ....
  56. ncbi request reprint Alpha-synuclein phosphorylation enhances eosinophilic cytoplasmic inclusion formation in SH-SY5Y cells
    Wanli W Smith
    Department of Psychiatry, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci 25:5544-52. 2005
    ..These results indicate that phosphorylation of alpha-synuclein at S129 may be important for the formation of inclusions in PD and related alpha synucleinopathies...
  57. ncbi request reprint Mitochondrial localization of the Parkinson's disease related protein DJ-1: implications for pathogenesis
    Li Zhang
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Hum Mol Genet 14:2063-73. 2005
    ..Our findings of DJ-1's mitochondrial localization may have important implications for understanding the pathogenesis of PD...
  58. ncbi request reprint Abeta deposition is associated with enhanced cortical alpha-synuclein lesions in Lewy body diseases
    Olga Pletnikova
    Department of Pathology Neuropathology, Johns Hopkins University School of Medicine, Ross Building 558, Baltimore, MD 21205, USA
    Neurobiol Aging 26:1183-92. 2005
    ..This suggests that Abeta enhances the development of cortical alpha-synuclein lesions in cases of PD...
  59. ncbi request reprint To die or grow: Parkinson's disease and cancer
    Andrew B West
    Institute for Cell Engineering, and Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Trends Neurosci 28:348-52. 2005
    ..When considering the normal function of these PD-linked genes in the periphery and their potential role in cancer, further emphasis might be placed on protein handling relating to cell-cycle control in the etiology of PD...
  60. ncbi request reprint Mediation of cell death by poly(ADP-ribose) polymerase-1
    David W Koh
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, 733 North Broadway St, Suite 711, Baltimore, MD 21205, USA
    Pharmacol Res 52:5-14. 2005
    ..Accordingly, modulation of PAR synthesis or degradation through the targeting of PARP-1 or PARG holds particular promise in the treatment of conditions such as cancer, stroke, and Parkinson's disease...
  61. ncbi request reprint Absence of inclusion body formation in the MPTP mouse model of Parkinson's disease
    Mika Shimoji
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, 733 North Broadway, Suite 731, Baltimore, MD 21205, USA
    Brain Res Mol Brain Res 134:103-8. 2005
    ..Our data showed that although there is a significant decrease in DA content and its metabolites and tyrosine hydroxylase immunoreactivity, there is no inclusion body formation following the various MPTP treatment regimens...
  62. ncbi request reprint Parkin mediates nonclassical, proteasomal-independent ubiquitination of synphilin-1: implications for Lewy body formation
    Kah Leong Lim
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci 25:2002-9. 2005
    ..Our results suggest that parkin is a dual-function ubiquitin ligase and that K63-linked ubiquitination of synphilin-1 by parkin may be involved in the formation of Lewy body inclusions associated with PD...
  63. pmc Aggregation promoting C-terminal truncation of alpha-synuclein is a normal cellular process and is enhanced by the familial Parkinson's disease-linked mutations
    Wenxue Li
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 102:2162-7. 2005
    ..Collectively, our results indicate that the biology behind the generation and accumulation of alpha-SynDeltaC is likely to have relevance for the initiation and the progression of alpha-Syn aggregation in vivo...
  64. ncbi request reprint Apoptosis-inducing factor substitutes for caspase executioners in NMDA-triggered excitotoxic neuronal death
    Hongmin Wang
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci 24:10963-73. 2004
    ..These results link PARP-1 activation with AIF translocation in NMDA-triggered excitotoxic neuronal death and provide a paradigm in which AIF can substitute for caspase executioners...
  65. ncbi request reprint Association of DJ-1 and parkin mediated by pathogenic DJ-1 mutations and oxidative stress
    Darren J Moore
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Hum Mol Genet 14:71-84. 2005
    ..These data potentially link DJ-1 and parkin in a common molecular pathway at multiple levels that may have important implications for understanding the pathogenesis of inherited and sporadic PD...
  66. ncbi request reprint Deadly conversations: nuclear-mitochondrial cross-talk
    Valina L Dawson
    Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    J Bioenerg Biomembr 36:287-94. 2004
    ..In exploiting this pathway for the development of new therapeutics, it will be important to block AIF translocation from the mitochondria to the nucleus without impairing important physiological functions of AIF in the mitochondria...
  67. ncbi request reprint Mechanism of neurodegenerative disease: role of the ubiquitin proteasome system
    Leonardo Petrucelli
    Mayo Clinic, Jacksonville, USA
    Ann Med 36:315-20. 2004
    ....
  68. pmc Human alpha-synuclein-harboring familial Parkinson's disease-linked Ala-53 --> Thr mutation causes neurodegenerative disease with alpha-synuclein aggregation in transgenic mice
    Michael K Lee
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205 2196, USA
    Proc Natl Acad Sci U S A 99:8968-73. 2002
    ..Further, alpha-Syn-dependent neurodegeneration is associated with abnormal accumulation of detergent-insoluble alpha-Syn...

Research Grants20

  1. Models of Familial Parkinson's Disease: PINK1
    Ted Dawson; Fiscal Year: 2006
    ....
  2. JHMI Clinical Center for Parkinson's Disease Neuroprotection Trials
    Ted Dawson; Fiscal Year: 2007
    ..abstract_text> ..
  3. The Role of Parkin in Parkinson's Disease
    Ted Dawson; Fiscal Year: 2007
    ....
  4. Reversible and Temporally Inducible LRRK2 Knockout Mice
    Ted Dawson; Fiscal Year: 2007
    ....
  5. The Role of Parkin in Parkinson's Disease
    Ted Dawson; Fiscal Year: 2009
    ....
  6. Apoptosis Inducing Factor in Dopaminergic Cell Death
    Ted Dawson; Fiscal Year: 2003
    ....
  7. The Role of Parkin in Parkinson's Disease
    Ted Dawson; Fiscal Year: 2004
    ....
  8. Models of Familial Parkinson's Disease: DJ-1 Knockouts
    Ted Dawson; Fiscal Year: 2005
    ....
  9. Poly (ADP-Ribose) and AIF in Neuronal Injury
    RAYMOND CHARLES KOEHLER; Fiscal Year: 2010
    ....