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      Adrenarche in nonhuman primates: the evidence for it and the need to redefine it

      , ,
      Journal of Endocrinology
      Bioscientifica

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          Abstract

          Adrenarche is most commonly defined as a prepubertal increase in circulating adrenal androgens, dehydroepiandrosterone (DHEA) and its sulfo-conjugate (DHEAS). This event is thought to have evolved in humans and some great apes but not in Old World monkeys, perhaps to promote brain development. Whether adrenarche represents a shared, derived developmental event in humans and our closest relatives, adrenal androgen secretion (and its regulation) is of considerable clinical interest. Specifically, adrenal androgens play a significant role in the pathophysiology of polycystic ovarian disease and breast and prostate cancers. Understanding the development of androgen secretion by the human adrenal cortex and identifying a suitable model for its study are therefore of central importance for clinical and evolutionary concerns. This review will examine the evidence for adrenarche in nonhuman primates (NHP) and suggest that a broader definition of this developmental event is needed, including morphological, biochemical, and endocrine criteria. Using such a definition, evidence from recent studies suggests that adrenarche evolved in Old World primates but spans a relatively brief period early in development compared with humans and some great apes. This emphasizes the need for frequent longitudinal sampling in evaluating developmental changes in adrenal androgen secretion as well as the tenuous nature of existing evidence of adrenarche in some species among the great apes. Central to an understanding of the regulation of adrenal androgen production in humans is the recognition of the complex nature of adrenarche and the need for more carefully conducted comparative studies and a broader definition in order to promote investigation among NHP in particular.

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          Most cited references94

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          Neurobiological and neuropsychiatric effects of dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS).

          DHEA and DHEAS are steroids synthesized in human adrenals, but their function is unclear. In addition to adrenal synthesis, evidence also indicates that DHEA and DHEAS are synthesized in the brain, further suggesting a role of these hormones in brain function and development. Despite intensifying research into the biology of DHEA and DHEAS, many questions concerning their mechanisms of action and their potential involvement in neuropsychiatric illnesses remain unanswered. We review and distill the preclinical and clinical data on DHEA and DHEAS, focusing on (i) biological actions and putative mechanisms of action, (ii) differences in endogenous circulating concentrations in normal subjects and patients with neuropsychiatric diseases, and (iii) the therapeutic potential of DHEA in treating these conditions. Biological actions of DHEA and DHEAS include neuroprotection, neurite growth, and antagonistic effects on oxidants and glucocorticoids. Accumulating data suggest abnormal DHEA and/or DHEAS concentrations in several neuropsychiatric conditions. The evidence that DHEA and DHEAS may be fruitful targets for pharmacotherapy in some conditions is reviewed.
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            Concurrent overproduction of synapses in diverse regions of the primate cerebral cortex.

            Synapses develop concurrently and at identical rates in different layers of the visual, somatosensory, motor, and prefrontal areas of the primate cerebral cortex. This isochronic course of synaptogenesis in anatomically and functionally diverse regions indicates that the entire cerebral cortex develops as a whole and that the establishment of cell-to-cell communication in this structure may be orchestrated by a single genetic or humoral signal. This is in contrast to the traditional view of hierarchical development of the cortical regions and provides new insight into the maturation of cortical functions.
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              Brain growth, life history, and cognition in primate and human evolution.

              S R Leigh (2004)
              This study investigates brain size ontogeny in a sample of seven anthropoid primate species (including humans) in order to evaluate longstanding ideas about the relations between brain size, brain ontogeny, life history, and cognition. First, this analysis tests the hypothesis that primate brain growth patterns vary across species. Second, the relations between the duration of the brain growth period and the duration of the pre-adult period are evaluated. Brain growth data, derived from a number of sources, are analyzed through parametric and nonparametric regressions. The results indicate that primates are characterized by significant variation in patterns of brain growth. In addition, the degree to which brain growth is allocated to either the pre- or the postnatal period varies substantially. Analyses of phylogenetically adjusted data show no correlation between the lengths of the brain growth period and the juvenile period, but there are correlations with other life-history variables. These results are explained in terms of maternal metabolic adaptations. Specifically, primates appear to present at least two major metabolic adaptations. In the first, brain growth occurs mainly during the prenatal period, reflecting heavy maternal investment. In the second, brain growth occupies large portions of the postnatal period. These differing patterns have important implications for maturation age, necessitating late maternal maturation in the first case and enabling relatively early maternal maturation in the second. Overall, these adaptations represent components of distinctive life-history adaptations, with potentially important implications for the evolution of primate cognition. Copyright 2004 Wiley-Liss, Inc.
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                Author and article information

                Journal
                Journal of Endocrinology
                Bioscientifica
                0022-0795
                1479-6805
                August 2012
                February 27 2012
                August 2012
                February 27 2012
                : 214
                : 2
                : 121-131
                Article
                10.1530/JOE-11-0467
                22378920
                e6cc7515-00b0-4499-b89c-38855ce8ee15
                © 2012

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