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Melatonin Prevents Death of Neuroblastoma Cells Exposed to the Alzheimer Amyloid Peptide

Miguel A. Pappolla, Melisa Sos, Rawhi A. Omar, Roger J. Bick, Diane L. M. Hickson-Bick, Russel J. Reiter, Spiros Efthimiopoulos and Nickolaos K. Robakis
Journal of Neuroscience 1 March 1997, 17 (5) 1683-1690; DOI: https://doi.org/10.1523/JNEUROSCI.17-05-01683.1997
Miguel A. Pappolla
1Department of Pathology and Laboratory Medicine, University of South Alabama, Mobile, Alabama 36617,
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Melisa Sos
2Department of Pathology and Laboratory Medicine, University of Texas Health Science Center at Houston, Houston, Texas 77030,
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Rawhi A. Omar
3Department of Pathology, University of Louisville, Louisville, Kentucky 40206,
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Roger J. Bick
2Department of Pathology and Laboratory Medicine, University of Texas Health Science Center at Houston, Houston, Texas 77030,
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Diane L. M. Hickson-Bick
2Department of Pathology and Laboratory Medicine, University of Texas Health Science Center at Houston, Houston, Texas 77030,
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Russel J. Reiter
4Department of Cellular and Structural Biology, The University of Texas Health Science Center, San Antonio, Texas 78229, and
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Spiros Efthimiopoulos
5Department of Psychiatry and Neurobiology, Mount Sinai School of Medicine, New York, New York 10029
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Nickolaos K. Robakis
5Department of Psychiatry and Neurobiology, Mount Sinai School of Medicine, New York, New York 10029
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Abstract

Studies from several laboratories have generated evidence suggesting that oxidative stress is involved in the pathogenesis of Alzheimer’s disease (AD). The finding that the amyloid β protein (Aβ) has neurotoxic properties and that such effects are, in part, mediated by free radicals has provided insights into mechanisms of cell death in AD and an avenue to explore new therapeutic approaches. In this study we demonstrate that melatonin, a pineal hormone with recently established antioxidant properties, is remarkably effective in preventing death of cultured neuroblastoma cells as well as oxidative damage and intracellular Ca2+ increases induced by a cytotoxic fragment of Aβ. The effects of melatonin were extremely reproducible and corroborated by multiple quantitative methods, including cell viability studies by confocal laser microscopy, electron microscopy, and measurements of intracellular calcium levels. The importance of this finding is that, in contrast to conventional antioxidants, melatonin has a proposed physiological role in the aging process. Secretion levels of this hormone are decreased in aging and more severely reduced in AD. The reported phenomenon may be of therapeutic relevance in AD.

  • Alzheimer’s disease
  • melatonin
  • Aβ toxicity
  • oxidative stress
  • neuronal cells
  • antioxidants
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The Journal of Neuroscience: 17 (5)
Journal of Neuroscience
Vol. 17, Issue 5
1 Mar 1997
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Melatonin Prevents Death of Neuroblastoma Cells Exposed to the Alzheimer Amyloid Peptide
Miguel A. Pappolla, Melisa Sos, Rawhi A. Omar, Roger J. Bick, Diane L. M. Hickson-Bick, Russel J. Reiter, Spiros Efthimiopoulos, Nickolaos K. Robakis
Journal of Neuroscience 1 March 1997, 17 (5) 1683-1690; DOI: 10.1523/JNEUROSCI.17-05-01683.1997

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Melatonin Prevents Death of Neuroblastoma Cells Exposed to the Alzheimer Amyloid Peptide
Miguel A. Pappolla, Melisa Sos, Rawhi A. Omar, Roger J. Bick, Diane L. M. Hickson-Bick, Russel J. Reiter, Spiros Efthimiopoulos, Nickolaos K. Robakis
Journal of Neuroscience 1 March 1997, 17 (5) 1683-1690; DOI: 10.1523/JNEUROSCI.17-05-01683.1997
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Keywords

  • Alzheimer’s disease
  • melatonin
  • Aβ toxicity
  • oxidative stress
  • neuronal cells
  • antioxidants

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