RT Journal Article
SR Electronic
T1 Melatonin Prevents Death of Neuroblastoma Cells Exposed to the Alzheimer Amyloid Peptide
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 1683
OP 1690
DO 10.1523/JNEUROSCI.17-05-01683.1997
VO 17
IS 5
A1 Miguel A. Pappolla
A1 Melisa Sos
A1 Rawhi A. Omar
A1 Roger J. Bick
A1 Diane L. M. Hickson-Bick
A1 Russel J. Reiter
A1 Spiros Efthimiopoulos
A1 Nickolaos K. Robakis
YR 1997
UL http://www.jneurosci.org/content/17/5/1683.abstract
AB 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.