Pineal melatonin rhythms and the timing of puberty in mammals

The direction of change in daylength provides the seasonal time cue for the timing of puberty in many mammalian species. The pattern of melatonin secretion from the pineal gland transduces the environmental light-dark cycle into a signal influencing the neuroendocrine control of sexual maturation. The change in duration of nocturnal melatonin secretion is probably the key feature of the melatonin signal which conveys daylength information. This information may also be used by neuroendocrine axes controlling seasonal changes in pelage colour, growth and metabolism. The mechanism of action of melatonin on neuroendocrine pathways is unknow. Although the ability to synthesize and secrete melatonin in a pattern that reflects the duration of the night may not occur until the postnatal period, the rodent and ovine foetus has the ability to respond in utero to photoperiodic cues to which its mother is exposed in late gestation. Transplacental passage of maternal melatonin is likely to be the mechanism by which photoperiodic cues reach the foetus. Species which do not exhibit seasonal patterns of puberty, such as the human, also secrete melatonin in a pattern which reflects the environmental light-dark cycle, but they do not respond reproductively to the seasonal melatonin information.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42811/1/18_2005_Article_BF01953052.pd

Oxidative Stress and Amyloid-Beta Pathology in Normal Individuals with A Maternal History of Alzheimer's

BACKGROUND: Epidemiology and imaging studies showed that cognitively normal (NL) individuals with a maternal history (MH) of late-onset Alzheimer’s disease (LOAD) may be at increased risk for AD compared to NL with a paternal history (PH) and NL with a negative family history of LOAD (NH). Using a panel of cerebrospinal fluid (CSF) markers, this study examined whether NL MH showed evidence for AD pathology compared to PH and NH. METHODS: Fifty-nine 40–80 year old NL subjects were examined, including 23 MH and 14 PH whose parents had a clinician-certified diagnosis of LOAD, and 22 NH. All subjects completed clinical, neuropsychological examinations and a lumbar puncture to measure CSF levels of amyloid-beta (Aβ(40), Aβ(42), Aβ(42/40)), total and hyperphosphorylated tau (T-Tau and P-Tau(231); markers of axonal degeneration and neurofibrillary tangles, respectively), and F(2)-isoprostanes (IsoP; a marker of oxidative stress). RESULTS: Groups were comparable for demographic and neuropsychological measures. MH subjects showed higher IsoP and reduced Aβ(42/40) CSF levels as compared to NH and to PH (P’s≤0.05), while no differences were found between NH and PH. No group differences were found for P-Tau(231) and T-Tau. IsoP and Aβ(42/40) levels were correlated only within the MH group (R(2)=0.32, P=0.005), and discriminated MH from the other subjects with 70% accuracy (relative risk=3.7, 95% confidence interval=1.6–9.7, P<0.001). Results remained significant controlling for age, gender, education, and ApoE genotype. CONCLUSIONS: Adult children of AD-affected mothers express a pathobiological phenotype characterized by Aβ-associated oxidative stress consistent with AD, which may reflect increased risk for developing the disease