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Melatonin increases survival and inhibits oxidative and amyloid pathology in a transgenic model of Alzheimer's disease.

Publication ,  Journal Article
Matsubara, E; Bryant-Thomas, T; Pacheco Quinto, J; Henry, TL; Poeggeler, B; Herbert, D; Cruz-Sanchez, F; Chyan, Y-J; Smith, MA; Perry, G ...
Published in: Journal of neurochemistry
June 2003

Increased levels of a 40-42 amino-acid peptide called the amyloid beta protein (A beta) 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 A beta-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 A beta, abnormal protein nitration, and survival of the mice. We report here that administration of melatonin partially inhibited the expected time-dependent elevation of beta-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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Published In

Journal of neurochemistry

DOI

EISSN

1471-4159

ISSN

0022-3042

Publication Date

June 2003

Volume

85

Issue

5

Start / End Page

1101 / 1108

Related Subject Headings

  • Survival Rate
  • Proteins
  • Oxidation-Reduction
  • Nitrates
  • Neurology & Neurosurgery
  • Mice, Transgenic
  • Mice
  • Melatonin
  • Humans
  • Disease Models, Animal
 

Citation

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Matsubara, E., Bryant-Thomas, T., Pacheco Quinto, J., Henry, T. L., Poeggeler, B., Herbert, D., … Neria, E. (2003). Melatonin increases survival and inhibits oxidative and amyloid pathology in a transgenic model of Alzheimer's disease. Journal of Neurochemistry, 85(5), 1101–1108. https://doi.org/10.1046/j.1471-4159.2003.01654.x
Matsubara, Etsuro, Tara Bryant-Thomas, Javier Pacheco Quinto, Tracey L. Henry, Burkhard Poeggeler, Donald Herbert, Felix Cruz-Sanchez, et al. “Melatonin increases survival and inhibits oxidative and amyloid pathology in a transgenic model of Alzheimer's disease.Journal of Neurochemistry 85, no. 5 (June 2003): 1101–8. https://doi.org/10.1046/j.1471-4159.2003.01654.x.
Matsubara E, Bryant-Thomas T, Pacheco Quinto J, Henry TL, Poeggeler B, Herbert D, et al. Melatonin increases survival and inhibits oxidative and amyloid pathology in a transgenic model of Alzheimer's disease. Journal of neurochemistry. 2003 Jun;85(5):1101–8.
Matsubara, Etsuro, et al. “Melatonin increases survival and inhibits oxidative and amyloid pathology in a transgenic model of Alzheimer's disease.Journal of Neurochemistry, vol. 85, no. 5, June 2003, pp. 1101–08. Epmc, doi:10.1046/j.1471-4159.2003.01654.x.
Matsubara E, Bryant-Thomas T, Pacheco Quinto J, Henry TL, Poeggeler B, Herbert D, Cruz-Sanchez F, Chyan Y-J, Smith MA, Perry G, Shoji M, Abe K, Leone A, Grundke-Ikbal I, Wilson GL, Ghiso J, Williams C, Refolo LM, Pappolla MA, Chain DG, Neria E. Melatonin increases survival and inhibits oxidative and amyloid pathology in a transgenic model of Alzheimer's disease. Journal of neurochemistry. 2003 Jun;85(5):1101–1108.
Journal cover image

Published In

Journal of neurochemistry

DOI

EISSN

1471-4159

ISSN

0022-3042

Publication Date

June 2003

Volume

85

Issue

5

Start / End Page

1101 / 1108

Related Subject Headings

  • Survival Rate
  • Proteins
  • Oxidation-Reduction
  • Nitrates
  • Neurology & Neurosurgery
  • Mice, Transgenic
  • Mice
  • Melatonin
  • Humans
  • Disease Models, Animal