KEVIN MCNAUGHT

Summary

Affiliation: Mount Sinai School of Medicine
Country: USA

Publications

  1. doi request reprint The pattern of neuronal loss and survival may reflect differential expression of proteasome activators in Parkinson's disease
    Kevin St P McNaught
    Department of Neurology, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    Synapse 64:241-50. 2010
  2. ncbi request reprint Impairment of the ubiquitin-proteasome system causes dopaminergic cell death and inclusion body formation in ventral mesencephalic cultures
    Kevin St P McNaught
    Department of Neurology, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Neurochem 81:301-6. 2002
  3. ncbi request reprint Selective loss of 20S proteasome alpha-subunits in the substantia nigra pars compacta in Parkinson's disease
    Kevin St P McNaught
    Department of Neurology, Mount Sinai School of Medicine, Annenberg 14 73, One Gustave L Levy Place, New York, NY 10029, USA
    Neurosci Lett 326:155-8. 2002
  4. ncbi request reprint Aggresome-related biogenesis of Lewy bodies
    Kevin St P McNaught
    Department of Neurology, Mount Sinai School of Medicine, Annenberg 14 73, One Gustave L Levy Place, New York, NY 10029, USA
    Eur J Neurosci 16:2136-48. 2002
  5. ncbi request reprint Systemic exposure to proteasome inhibitors causes a progressive model of Parkinson's disease
    Kevin St P McNaught
    Department of Neurology, Neuropathology Division, Mount Sinai School of Medicine, New York, NY 10029, USA
    Ann Neurol 56:149-62. 2004
  6. ncbi request reprint Brainstem pathology in DYT1 primary torsion dystonia
    Kevin St P McNaught
    Department of Neurology, Neuropathology Division, Mount Sinai School of Medicine, New York, NY 10029, USA
    Ann Neurol 56:540-7. 2004
  7. ncbi request reprint Protein aggregation in the pathogenesis of familial and sporadic Parkinson's disease
    Kevin St P McNaught
    Department of Neurology, Mount Sinai School of Medicine, Annenberg 14 73, One Gustave L Levy Place, New York, NY 10029, USA
    Neurobiol Aging 27:530-45. 2006
  8. ncbi request reprint Proteasomal dysfunction in sporadic Parkinson's disease
    Kevin St P McNaught
    Department of Neurology, Mount Sinai School of Medicine, New York, NY 10029, USA
    Neurology 66:S37-49. 2006
  9. ncbi request reprint Proteasome inhibitor-induced model of Parkinson's disease
    Kevin St P McNaught
    Department of Neurology, Mount Sinai School of Medicine, New York, NY, USA
    Ann Neurol 60:243-7. 2006

Research Grants

Detail Information

Publications9

  1. doi request reprint The pattern of neuronal loss and survival may reflect differential expression of proteasome activators in Parkinson's disease
    Kevin St P McNaught
    Department of Neurology, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    Synapse 64:241-50. 2010
    ..Thus, the differential distribution and activity of proteasome activations could play a significant role in the pathogenesis of PD...
  2. ncbi request reprint Impairment of the ubiquitin-proteasome system causes dopaminergic cell death and inclusion body formation in ventral mesencephalic cultures
    Kevin St P McNaught
    Department of Neurology, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Neurochem 81:301-6. 2002
    ..This study supports the concept that defects in the UPS may underlie nigral pathology in familial and sporadic forms of PD...
  3. ncbi request reprint Selective loss of 20S proteasome alpha-subunits in the substantia nigra pars compacta in Parkinson's disease
    Kevin St P McNaught
    Department of Neurology, Mount Sinai School of Medicine, Annenberg 14 73, One Gustave L Levy Place, New York, NY 10029, USA
    Neurosci Lett 326:155-8. 2002
    ..Thus, structural and function defects in 26/20S proteasomes may underlie protein accumulation, formation of proteinaceous Lewy bodies and dopaminergic neuronal death in the SNc in sporadic PD...
  4. ncbi request reprint Aggresome-related biogenesis of Lewy bodies
    Kevin St P McNaught
    Department of Neurology, Mount Sinai School of Medicine, Annenberg 14 73, One Gustave L Levy Place, New York, NY 10029, USA
    Eur J Neurosci 16:2136-48. 2002
    ..This phenomenon is consistent with growing evidence that altered protein handling underlies the etiopathogenesis of PD and related disorders...
  5. ncbi request reprint Systemic exposure to proteasome inhibitors causes a progressive model of Parkinson's disease
    Kevin St P McNaught
    Department of Neurology, Neuropathology Division, Mount Sinai School of Medicine, New York, NY 10029, USA
    Ann Neurol 56:149-62. 2004
    ..This animal model induced by proteasome inhibitors closely recapitulates key features of PD and may be valuable in studying etiopathogenic mechanisms and putative neuroprotective therapies for the illness...
  6. ncbi request reprint Brainstem pathology in DYT1 primary torsion dystonia
    Kevin St P McNaught
    Department of Neurology, Neuropathology Division, Mount Sinai School of Medicine, New York, NY 10029, USA
    Ann Neurol 56:540-7. 2004
    ..and cuneiform nuclei, and related brainstem brainstem structures, in mediating motor activity and controlling muscle tone suggests that alterations in these structures could underlie the pathophysiology of DYT1 dystonia [corrected]..
  7. ncbi request reprint Protein aggregation in the pathogenesis of familial and sporadic Parkinson's disease
    Kevin St P McNaught
    Department of Neurology, Mount Sinai School of Medicine, Annenberg 14 73, One Gustave L Levy Place, New York, NY 10029, USA
    Neurobiol Aging 27:530-45. 2006
    ..This suggests that manipulation of proteolytic systems is a rational approach in the development of neuroprotective therapies that could modify the pathological course of PD...
  8. ncbi request reprint Proteasomal dysfunction in sporadic Parkinson's disease
    Kevin St P McNaught
    Department of Neurology, Mount Sinai School of Medicine, New York, NY 10029, USA
    Neurology 66:S37-49. 2006
    ..It remains to be established if proteasomal dysfunction plays a primary or a secondary role in the initiation or progression of the neurodegenerative process in PD...
  9. ncbi request reprint Proteasome inhibitor-induced model of Parkinson's disease
    Kevin St P McNaught
    Department of Neurology, Mount Sinai School of Medicine, New York, NY, USA
    Ann Neurol 60:243-7. 2006
    ..We have begun to examine various factors that alone or in combination might explain these differences, and we present in this article preliminary results from these studies...

Research Grants5

  1. ROLE OF PROTEASOMAL DYSFUNCTION IN PARKINSON'S DISEASE
    KEVIN MCNAUGHT; Fiscal Year: 2007
    ..These studies will test our hypothesis that inadequate proteasomal function underlies both vulnerability and degeneration of the SNc in sporadic Parkinson's disease. ..