The DOI matches its Crossref record; 62 of the 63 references it cites were found in a registry or an index.
Melatonin Prevents Death of Neuroblastoma Cells Exposed to the Alzheimer Amyloid Peptide
Open accessAbstract
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 beta protein (Abeta) 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 Abeta. 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.
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“Studies have also reported that antioxidants protect against Aβ induced neuronal toxicity [16,17].”
From Indian Medicinal Herbs and Formulations for Alzheimer’s Disease, from Traditional Knowledge to Scientific Assessment (2020) · cites this paper as [17]
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Cites
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Hydrogen peroxide mediates amyloid β protein toxicity
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Neurotrophic and Neurotoxic Effects of Amyloid β Protein: Reversal by Tachykinin Neuropeptides
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Amyloid β-peptide is produced by cultured cells during normal metabolism
Haass, C., Schlossmacher, M. G., Hung, A. Y., Vigo-Pelfrey, C., Mellon, A., Ostaszewski, B. L., Lieberburg, I., Koo, E. H., Schenk, D., Teplow, D. B., et al. (1992) · Nature · doi:10.1038/359322a0 · Cited by 1,921 · cited 1×
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“In addition to free radicals, increased sensitivity to excitotoxicity (Copani et al., 1995) and /or disruption of Ca 2ϩ homeostasis (Mattson et al., 1992, 1993; Le et al., 1995; Mark et al., 1995) seem to be involved.”
BackgroundFluorescent indicators for cytosolic calcium based on rhodamine and fluorescein chromophores
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Research works printed but not linked: 1
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Oxidative stress and Alzheimer disease
Christen, Y. (2000) · American Journal of Clinical Nutrition · doi:10.1093/ajcn/71.2.621s · Cited by 1,176
Melatonin as a natural ally against oxidative stress: a physicochemical examination
Galano, A., Tan, D. X., & Reiter, R. J. (2011) · Journal of Pineal Research · doi:10.1111/j.1600-079x.2011.00916.x · Cited by 1,167
Oxidative damage in the central nervous system: protection by melatonin
Reiter, R. J. (1998) · Progress in Neurobiology · doi:10.1016/s0301-0082(98)00052-5 · Cited by 836
“In addition, Pappolla et al. (1997c, 1998) have recently found that the aggregation of Ab peptide into b-sheets and amyloid ®brils, which are important for the toxicity of the peptide and renders it resistance to proteolytic degradation, is greatly reduced by melatonin.”
BackgroundNeuropathogenesis of Delirium: Review of Current Etiologic Theories and Common Pathways
Maldonado, J. R. (2013) · The American Journal of Geriatric Psychiatry · doi:10.1016/j.jagp.2013.09.005 · Cited by 745
Bioinorganic Chemistry of Alzheimer’s Disease
Kepp, K. P. (2012) · Chemical Reviews · doi:10.1021/cr300009x · Cited by 683
Metadata
- Authors
- Pappolla, M. A., Sos, M., Omar, R. A., Bick, R. J., Hickson-Bick, D. L. M., Reiter, R. J., Efthimiopoulos, S., & Robakis, N. K.
- Affiliations
- University of South Alabama (US)
- The University of Texas Health Science Center at Houston (US)
- University of Louisville (US)
- The University of Texas at San Antonio Health Science Center (US)
- Icahn School of Medicine at Mount Sinai (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1997-03-01
- Volume
- 17
- Issue
- 5
- Pages
- 1683-1690
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6573387
- OpenAlex
- W2137034584
- Cited by
- 359
- References
- 63
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 4 · 2023: 4 · 2022: 3 · 2021: 4 · 2020: 9 · 2019: 6 · 2018: 12 · 2017: 5 · 2016: 9 · 2015: 7 · 2014: 16 · 2013: 15 · 2012: 14
- FWCI
- 8.23
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ag011130-03)
- National Institute on Aging (RF1AG008200, R56AG008200, AG-08200, AG-11130, R01AG008200)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- melatonin, Alzheimer's disease, amyloid-beta, neuroblastoma cells, oxidative stress, neurotoxicity, cell death, intracellular calcium, aging, pineal hormone
- MeSH terms
- Alzheimer Disease, Animals, Antioxidants, Calcium, Ditiocarb, Doxorubicin, Melatonin, Neuroblastoma, Neurons, Peptide Fragments, Peptides, Superoxide Dismutase, Reproducibility of Results, Lipid Peroxidation, Amyloid beta-Peptides, PC12 Cells, Apoptosis, Oxidative Stress, Mice, Rats
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