Melatonin increases survival and inhibits oxidative and amyloid pathology in a transgenic model of Alzheimer's disease
Abstract
Increased levels of a 40–42 amino‐acid peptide called the amyloid β protein (Aβ) and evidence of oxidative damage are early neuropathological markers of Alzheimer's disease (AD). Previous investigations have demonstrated that melatonin is decreased during the aging process and that patients with AD have more profound reductions of this hormone. It has also been recently shown that melatonin protects neuronal cells from Aβ‐mediated oxidative damage and inhibits the formation of amyloid fibrils in vitro. However, a direct relationship between melatonin and the biochemical pathology of AD had not been demonstrated. We used a transgenic mouse model of Alzheimer's amyloidosis and monitored over time the effects of administering melatonin on brain levels of Aβ, abnormal protein nitration, and survival of the mice. We report here that administration of melatonin partially inhibited the expected time‐dependent elevation of β‐amyloid, reduced abnormal nitration of proteins, and increased survival in the treated transgenic mice. These findings may bear relevance to the pathogenesis and therapy of AD.
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Melatonin in AD has been validated by in vivo and in vitro studies demonstrating a beneficial effect in reducing Aβ generation and deposition.
“Melatonin in AD has been validated by in vivo and in vitro studies demonstrating also a beneficial effect in reducing Aβ generation and deposition.79”
From From combinations to multitarget-directed ligands: A continuum in Alzheimer’s disease polypharmacology (2021) · cites this paper as [79]
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- Authors
- Matsubara, E., Bryant‐Thomas, T., Pacheco Quinto, J., Henry, T. L., Poeggeler, B., Herbert, D., Cruz‐Sanchez, F., Chyan, Y., Smith, M. A., Perry, G., Shoji, M., Abe, K., Leone, A., Grundke‐Ikbal, I., Wilson, G. L., Ghiso, J., Williams, C., Refolo, L. M., & Pappolla, M. A.
- Affiliations
- Okayama University (JP)
- University of South Alabama (US)
- Case Western Reserve University (US)
- New York University (US)
- Duke University (US)
- Alzheimer's Drug Discovery Foundation (US)
- Corresponding author
- Pappolla, Miguel A.
- ORCID
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2003-05-14
- Volume
- 85
- Issue
- 5
- Pages
- 1101-1108
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W1981359936
- Cited by
- 332
- References
- 53
- Citations by year
- 2026: 4 · 2025: 10 · 2024: 16 · 2023: 14 · 2022: 10 · 2021: 13 · 2020: 16 · 2019: 20 · 2018: 9 · 2017: 8 · 2016: 13 · 2015: 14 · 2014: 13 · 2013: 19 · 2012: 19
- FWCI
- 12.46
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R01AG016783, R01 AG16783-04)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- melatonin, Alzheimer's disease, amyloid-beta, oxidative stress, protein nitration, amyloidosis, transgenic mouse model, survival, neuroprotection, amyloid fibril formation
- MeSH terms
- Alzheimer Disease, Amyloidosis, Animals, Disease Models, Animal, Humans, Melatonin, Mice, Transgenic, Nitrates, Oxidation-Reduction, Proteins, Survival Rate, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Mice
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