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Volume 17, Number 5,
Issue of March 1, 1997
pp. 1683-1690
Copyright ©1997 Society for Neuroscience
Melatonin Prevents Death of Neuroblastoma Cells Exposed to the
Alzheimer Amyloid Peptide
Received Sept. 27, 1996; revised Dec. 4, 1996; accepted Dec. 16, 1996.
Miguel A. Pappolla1,
Melisa Sos2,
Rawhi A. Omar3,
Roger J. Bick2,
Diane L. M. Hickson-Bick2,
Russel J. Reiter4,
Spiros Efthimiopoulos5, and
Nickolaos K. Robakis5
1 Department of Pathology and Laboratory Medicine,
University of South Alabama, Mobile, Alabama 36617, 2 Department of Pathology and Laboratory Medicine,
University of Texas Health Science Center at Houston, Houston, Texas
77030, 3 Department of Pathology, University of Louisville,
Louisville, Kentucky 40206, 4 Department of Cellular and
Structural Biology, The University of Texas Health Science Center, San
Antonio, Texas 78229, and 5 Department of Psychiatry and
Neurobiology, Mount Sinai School of Medicine, New York, New York
10029
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  protein (A) 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 A. 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.
Key words:
Alzheimer's disease;
melatonin;
A toxicity;
oxidative
stress;
neuronal cells;
antioxidants
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