Melatonin, metals, and gene expression: Implications in aging and neurodegenerative disorders

Debomoy Lahiri, Demao Chen, Preeti Lahiri, Jack T. Rogers, Nigel H. Greig, Stephen Bondy

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Melatonin is a hormone secreted by the pineal gland, mostly in the dark period of the light/dark cycle, with corresponding fluctuations reflected in the plasma melatonin levels. This hormone plays a critical role in the regulation of various neural and endocrine processes that are synchronized with daily change in photoperiod. Abnormal melatonin levels are associated with metabolic disturbances and other disorders. Melatonin potentially plays an important role in aging, prolongation of life span, and health in the aged individual. It may exert a beneficial action on neurodegenerative conditions in those with debilitating diseases. It interacts with metals and, in some cases, neutralizes their toxic effects. Levels of melatonin decrease with aging in mice. Its dietary supplementation has recently been shown to result in a significant rise in levels of endogenous melatonin in serum as well as all other tissue samples tested. The effects of dietary melatonin have been studied in the brain of mice with regard to nitric oxide synthase, synaptic proteins, and amyloid β peptides (Aβ), which are involved in amyloid deposition and plaque formation in Alzheimer's disease (AD). Melatonin supplementation has no significant effect on cerebral cortical levels of nitric oxide synthase or synaptic proteins, such as synaptophysin and SNAP-25. Notably, however, elevated brain melatonin levels resulted in a significant reduction in levels of toxic cortical Aβ of both 40- and 42-aminoacid forms. Taken together, these results suggest that dietary melatonin supplementation may slow the neurodegenerative changes associated with brain aging and that the depletion of melatonin in the brain of aging mice may, in part, account for this adverse change.

Original languageEnglish
Pages (from-to)216-230
Number of pages15
JournalAnnals of the New York Academy of Sciences
Volume1035
DOIs
StatePublished - 2004

Fingerprint

Melatonin
Gene expression
Neurodegenerative Diseases
Aging of materials
Metals
Gene Expression
Brain
Poisons
Photoperiod
Dietary Supplements
Nitric Oxide Synthase
Hormones
Life Support Care
Amyloidogenic Proteins
Synaptophysin
Mouse
Pineal Gland
Amyloid Plaques
Amyloid
Alzheimer Disease

Keywords

  • Aging
  • Amyloid
  • Brain
  • Diet
  • Melatonin
  • Metals
  • Mouse
  • mRNA
  • Synaptic protein

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Melatonin, metals, and gene expression : Implications in aging and neurodegenerative disorders. / Lahiri, Debomoy; Chen, Demao; Lahiri, Preeti; Rogers, Jack T.; Greig, Nigel H.; Bondy, Stephen.

In: Annals of the New York Academy of Sciences, Vol. 1035, 2004, p. 216-230.

Research output: Contribution to journalArticle

Lahiri, Debomoy ; Chen, Demao ; Lahiri, Preeti ; Rogers, Jack T. ; Greig, Nigel H. ; Bondy, Stephen. / Melatonin, metals, and gene expression : Implications in aging and neurodegenerative disorders. In: Annals of the New York Academy of Sciences. 2004 ; Vol. 1035. pp. 216-230.
@article{93886d5443ba494bb28c1d2b9d6adbc3,
title = "Melatonin, metals, and gene expression: Implications in aging and neurodegenerative disorders",
abstract = "Melatonin is a hormone secreted by the pineal gland, mostly in the dark period of the light/dark cycle, with corresponding fluctuations reflected in the plasma melatonin levels. This hormone plays a critical role in the regulation of various neural and endocrine processes that are synchronized with daily change in photoperiod. Abnormal melatonin levels are associated with metabolic disturbances and other disorders. Melatonin potentially plays an important role in aging, prolongation of life span, and health in the aged individual. It may exert a beneficial action on neurodegenerative conditions in those with debilitating diseases. It interacts with metals and, in some cases, neutralizes their toxic effects. Levels of melatonin decrease with aging in mice. Its dietary supplementation has recently been shown to result in a significant rise in levels of endogenous melatonin in serum as well as all other tissue samples tested. The effects of dietary melatonin have been studied in the brain of mice with regard to nitric oxide synthase, synaptic proteins, and amyloid β peptides (Aβ), which are involved in amyloid deposition and plaque formation in Alzheimer's disease (AD). Melatonin supplementation has no significant effect on cerebral cortical levels of nitric oxide synthase or synaptic proteins, such as synaptophysin and SNAP-25. Notably, however, elevated brain melatonin levels resulted in a significant reduction in levels of toxic cortical Aβ of both 40- and 42-aminoacid forms. Taken together, these results suggest that dietary melatonin supplementation may slow the neurodegenerative changes associated with brain aging and that the depletion of melatonin in the brain of aging mice may, in part, account for this adverse change.",
keywords = "Aging, Amyloid, Brain, Diet, Melatonin, Metals, Mouse, mRNA, Synaptic protein",
author = "Debomoy Lahiri and Demao Chen and Preeti Lahiri and Rogers, {Jack T.} and Greig, {Nigel H.} and Stephen Bondy",
year = "2004",
doi = "10.1196/annals.1332.014",
language = "English",
volume = "1035",
pages = "216--230",
journal = "Annals of the New York Academy of Sciences",
issn = "0077-8923",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - Melatonin, metals, and gene expression

T2 - Implications in aging and neurodegenerative disorders

AU - Lahiri, Debomoy

AU - Chen, Demao

AU - Lahiri, Preeti

AU - Rogers, Jack T.

AU - Greig, Nigel H.

AU - Bondy, Stephen

PY - 2004

Y1 - 2004

N2 - Melatonin is a hormone secreted by the pineal gland, mostly in the dark period of the light/dark cycle, with corresponding fluctuations reflected in the plasma melatonin levels. This hormone plays a critical role in the regulation of various neural and endocrine processes that are synchronized with daily change in photoperiod. Abnormal melatonin levels are associated with metabolic disturbances and other disorders. Melatonin potentially plays an important role in aging, prolongation of life span, and health in the aged individual. It may exert a beneficial action on neurodegenerative conditions in those with debilitating diseases. It interacts with metals and, in some cases, neutralizes their toxic effects. Levels of melatonin decrease with aging in mice. Its dietary supplementation has recently been shown to result in a significant rise in levels of endogenous melatonin in serum as well as all other tissue samples tested. The effects of dietary melatonin have been studied in the brain of mice with regard to nitric oxide synthase, synaptic proteins, and amyloid β peptides (Aβ), which are involved in amyloid deposition and plaque formation in Alzheimer's disease (AD). Melatonin supplementation has no significant effect on cerebral cortical levels of nitric oxide synthase or synaptic proteins, such as synaptophysin and SNAP-25. Notably, however, elevated brain melatonin levels resulted in a significant reduction in levels of toxic cortical Aβ of both 40- and 42-aminoacid forms. Taken together, these results suggest that dietary melatonin supplementation may slow the neurodegenerative changes associated with brain aging and that the depletion of melatonin in the brain of aging mice may, in part, account for this adverse change.

AB - Melatonin is a hormone secreted by the pineal gland, mostly in the dark period of the light/dark cycle, with corresponding fluctuations reflected in the plasma melatonin levels. This hormone plays a critical role in the regulation of various neural and endocrine processes that are synchronized with daily change in photoperiod. Abnormal melatonin levels are associated with metabolic disturbances and other disorders. Melatonin potentially plays an important role in aging, prolongation of life span, and health in the aged individual. It may exert a beneficial action on neurodegenerative conditions in those with debilitating diseases. It interacts with metals and, in some cases, neutralizes their toxic effects. Levels of melatonin decrease with aging in mice. Its dietary supplementation has recently been shown to result in a significant rise in levels of endogenous melatonin in serum as well as all other tissue samples tested. The effects of dietary melatonin have been studied in the brain of mice with regard to nitric oxide synthase, synaptic proteins, and amyloid β peptides (Aβ), which are involved in amyloid deposition and plaque formation in Alzheimer's disease (AD). Melatonin supplementation has no significant effect on cerebral cortical levels of nitric oxide synthase or synaptic proteins, such as synaptophysin and SNAP-25. Notably, however, elevated brain melatonin levels resulted in a significant reduction in levels of toxic cortical Aβ of both 40- and 42-aminoacid forms. Taken together, these results suggest that dietary melatonin supplementation may slow the neurodegenerative changes associated with brain aging and that the depletion of melatonin in the brain of aging mice may, in part, account for this adverse change.

KW - Aging

KW - Amyloid

KW - Brain

KW - Diet

KW - Melatonin

KW - Metals

KW - Mouse

KW - mRNA

KW - Synaptic protein

UR - http://www.scopus.com/inward/record.url?scp=14944371728&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=14944371728&partnerID=8YFLogxK

U2 - 10.1196/annals.1332.014

DO - 10.1196/annals.1332.014

M3 - Article

C2 - 15681810

AN - SCOPUS:14944371728

VL - 1035

SP - 216

EP - 230

JO - Annals of the New York Academy of Sciences

JF - Annals of the New York Academy of Sciences

SN - 0077-8923

ER -