Normative data on the daily profile of urinary 6-sulfatoxymelatonin in healthy subjects between the ages of 20 and 84

Mahlberg, Richard; Tilmann, Amely; Salewski, Lothar; Kunz, Dieter

doi:10.1016/j.psyneuen.2006.01.009

Cited by 90 publications

(55 citation statements)

References 53 publications

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“…Nevertheless, the values included here, obtained from samples taken in the early morning, are longitudinal (two measurements in the same subject, separated by one pubertal stage, approximately 1 year). Although melatonin levels tend to be higher in females throughout the lifespan [24, 25], only one previous paper from our group recorded differences during adolescence in the concentration of melatonin according to gender [4]; the results of the present study confirm that during puberty the values of serum melatonin tend to be higher in females. In addition, the variation between measurements was also greater among females, although without reaching statistical significance.…”

Section: Discussionsupporting

confidence: 79%

Longitudinal Study of the Simultaneous Secretion of Melatonin and Leptin during Normal Puberty

Molina-Carballo

Fernández-Tardáguila²,

Uberos‐Fernández³

et al. 2007

Horm Res Paediatr

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Background/Aims: Pubertal changes are a consequence of the activation of the hypothalamic-pituitary-gonadal axis due to an increase in the frequency and magnitude of pulses of gonadotropin-releasing hormone (GnRH), which may depend on the intrinsic properties of the neurons of the hypothalamic arcuatus nucleus, or on the influence of neurotransmitters and/or neuromodulators. We evaluated the serum concentrations of melatonin and leptin in healthy prepubertal and adolescent subjects of both sexes, to define their participation at the initial stages and during the progression of pubertal development. Methods: 80 pediatric subjects (47 females and 33 males), aged 6–18 years, were divided into 2 groups, prepubertal (n = 25) and adolescent (n = 55), according to the absence or presence, respectively, of physical signs of pubertal development. The subjects were assessed on two occasions: at the time of their inclusion in the study, and 12–18 months later when the subject had advanced one pubertal stage according to the Tanner classification. Blood was obtained in fasting for clinical purposes and for the hormonal study. Melatonin and leptin were measured by radioimmunoanalysis. Results: As described previously, melatonin decreases at the onset of puberty and during pubertal development. Both the absolute melatonin value and the decrease between evaluations tended to be greater in females; the variations were correlated with neither an increase in body weight nor with the degree of pubertal development. The concentration of leptin increased in both sexes with the progression of puberty, this value being 40% greater in women, and correlated with the indicators of an increase in body volume and fat accumulation. Although its concentration remained stable between evaluations for both sexes, among the males the association between leptin and pubertal development took place at the start of the process, while for the females we observed a significant overall association between pubertal stage and leptin concentration, this association being stronger at more advanced Tanner stages. Neither at the onset of puberty nor during its course did we observe any significant relation between melatonin concentration and any of the Tanner stages, whether for males or for females. Neither was there any correlation between the absolute values or rates of modification of melatonin and leptin. Conclusion: According to the evolutionary dynamics of their respective concentrations, both initially and during pubertal progress, melatonin and leptin do not interact in the initiation or progression of human pubertal development, and do not seem to play a key role in this process.

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Section: Discussionsupporting

confidence: 79%

Longitudinal Study of the Simultaneous Secretion of Melatonin and Leptin during Normal Puberty

Molina-Carballo

Fernández-Tardáguila²,

Uberos‐Fernández³

et al. 2007

Horm Res Paediatr

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“…In the central nervous system, melatonin is cleaved to other metabolites, such as N 1 -acetyl-N 2 -formyl-5-methoxykynuramine (AFMK) and N 1 -acetyl-5-methoxykynuramine (AMK) (54), which are well-documented scavengers (55). The secretion of melatonin metabolites, including 6-sulfatoxymelatonin, declines in aged individuals (56). Similar to the melatonin pathway from production to degradation, a significant age-associated functional decline is observed, and this decline may contribute to the reduction of melatonin levels during aging.…”

Section: Melatonin During Agingmentioning

confidence: 99%

Effects of Melatonin on Nervous System Aging: Neurogenesis and Neurodegeneration

et al. 2013

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Abstract. Neural aging as a progressive loss of function involves central and peripheral postmitotic neurons and neural stem cells (NSCs). It promotes neurodegeneration, impairs neurogenesis, and can be considered a cause of cognitive impairment and sensory and motor deficits in the elderly. Age-related morphological atrophic changes and cellular alterations are addressed by neural aging mechanisms. Neurogenesis declines during aging through several mechanisms such as an increase in quiescence state, changes in lineage fate, telomerase dysfunction, the failure of the DNA repair system, increased apoptosis, and the impairment of self-renewal. The selfrenewal transcriptional factor Sox2 has been correlated with retrotransposon L1 and certain cellcycle-and epigenetic-related factors, which are sometimes considered age-related factors in NSC aging. As neurogenesis decreases, non-mitotic neurons undergo neurodegeneration by oxidative stress, sirtuin, insulin signaling and mTOR alteration, mitochondrial dysfunction, and protein misfolding and aggregation. As neurodegeneration and impaired neurogenesis promote the nervous system aging process, the identification of neuronal anti-aging is required to raise life expectancy. The role of melatonin in increasing neurogenesis and protecting against neurodegeneration has been investigated. Here, we review nervous system aging that is correlated with mechanisms of neurodegeneration and the impairment of neurogenesis and evaluate the effects of melatonin on these processes.

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“…The deterioration is accompanied by a decrease in circadian amplitude, evidenced by sleep loss at night and difficulty staying awake during the day (Turek et al, 1995;Dijk et al, 1999;Hofman and Swaab, 2006). Nearly all measured physiological functions show a decrease in rhythm amplitude, including temperature and melatonin rhythms (Dijk et al, 1999;Mahlberg et al, 2006). Implantation of neonatal SCN tissue into aged hamsters improves circadian rhythmicity and increases longevity (Hurd and Ralph, 1998), indicating that proper functioning of the SCN is crucial for healthy aging.…”

Section: Introductionmentioning

confidence: 99%

Evidence for Neuronal Desynchrony in the Aged Suprachiasmatic Nucleus Clock

Farajnia¹,

Michel²,

Deboer³

et al. 2012

J. Neurosci.

198

212

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Aging is associated with a deterioration of daily (circadian) rhythms in physiology and behavior. Deficits in the function of the central circadian pacemaker in the suprachiasmatic nucleus (SCN) have been implicated, but the responsible mechanisms have not been clearly delineated. In this report, we characterize the progression of rhythm deterioration in mice to 900 d of age. Longitudinal behavioral and sleep-wake recordings in up to 30-month-old mice showed strong fragmentation of rhythms, starting at the age of 700 d. Patch-clamp recordings in this age group revealed deficits in membrane properties and GABAergic postsynaptic current amplitude. A selective loss of circadian modulation of fast delayed-rectifier and A-type K ϩ currents was observed. At the tissue level, phase synchrony of SCN neurons was grossly disturbed, with some subpopulations peaking in anti-phase and a reduction in amplitude of the overall multiunit activity rhythm. We propose that aberrant SCN rhythmicity in old animals-with electrophysiological arrhythmia at the single-cell level and phase desynchronization at the network level-can account for defective circadian function with aging.

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Normative data on the daily profile of urinary 6-sulfatoxymelatonin in healthy subjects between the ages of 20 and 84

Cited by 90 publications

References 53 publications

Longitudinal Study of the Simultaneous Secretion of Melatonin and Leptin during Normal Puberty

Longitudinal Study of the Simultaneous Secretion of Melatonin and Leptin during Normal Puberty

Effects of Melatonin on Nervous System Aging: Neurogenesis and Neurodegeneration

Evidence for Neuronal Desynchrony in the Aged Suprachiasmatic Nucleus Clock

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