The Experts below are selected from a list of 80535 Experts worldwide ranked by ideXlab platform

John J. Mcgrath - One of the best experts on this subject based on the ideXlab platform.

  • Developmental vitamin D deficiency causes abnormal Brain Development.
    Psychoneuroendocrinology, 2009
    Co-Authors: Darryl W. Eyles, Francois Feron, John J. Mcgrath, X. Cui, J. P. Kesby, L. H. Harms, Thomas H. J. Burne
    Abstract:

    There is now clear evidence that vitamin D is involved in Brain Development. Our group is interested in environmental factors that shape Brain Development and how this may be relevant to neuropsychiatric diseases including schizophrenia. The origins of schizophrenia are considered Developmental. We hypothesised that Developmental vitamin D (DVD) deficiency may be the plausible neurobiological explanation for several important epidemiological correlates of schizophrenia namely: (1) the excess winter/spring birth rate, (2) increased incidence of the disease in 2nd generation Afro-Caribbean migrants and (3) increased urban birth rate. Moreover we have published two pieces of direct epidemiological support for this hypothesis in patients. In order to establish the "Biological Plausibility" of this hypothesis we have developed an animal model to study the effect of DVD deficiency on Brain Development. We do this by removing vitamin D from the diet of female rats prior to breeding. At birth we return all dams to a vitamin D containing diet. Using this procedure we impose a transient, gestational vitamin D deficiency, while maintaining normal calcium levels throughout. The Brains of offspring from DVD-deficient dams are characterised by (1) a mild distortion in Brain shape, (2) increased lateral ventricle volumes, (3) reduced differentiation and (4) diminished expression of neurotrophic factors. As adults, the alterations in ventricular volume persist and alterations in Brain gene and protein expression emerge. Adult DVD-deficient rats also display behavioural sensitivity to agents that induce psychosis (the NMDA antagonist MK-801) and have impairments in attentional processing. In this review we summarise the literature addressing the function of vitamin D on neuronal and non-neuronal cells as well as in vivo results from DVD-deficient animals. Our conclusions from these data are that vitamin D is a plausible biological risk factor for neuropsychiatric disorders and that vitamin D acts as a neurosteroid with direct effects on Brain Development.

  • Schizophrenia, vitamin D, and Brain Development.
    International review of neurobiology, 2004
    Co-Authors: Alan Mackay-sim, Francois Feron, Darryl W. Eyles, Thomas H. J. Burne, John J. Mcgrath
    Abstract:

    Schizophrenia research is invigorated at present by the recent discovery of several plausible candidate susceptibility genes identified from genetic linkage and gene expression studies of Brains from persons with schizophrenia. It is a current challenge to reconcile this gathering evidence for specific candidate susceptibility genes with the "neuroDevelopmental hypothesis," which posits that schizophrenia arises from gene-environment interactions that disrupt Brain Development. We make the case here that schizophrenia may result not from numerous genes of small effect, but a few genes of transcriptional regulation acting during Brain Development. In particular we propose that low vitamin D during Brain Development interacts with susceptibility genes to alter the trajectory of Brain Development, probably by epigenetic regulation that alters gene expression throughout adult life. Vitamin D is an attractive "environmental" candidate because it appears to explain several key epidemiological features of schizophrenia. Vitamin D is an attractive "genetic" candidate because its nuclear hormone receptor regulates gene expression and nervous system Development. The polygenic quality of schizophrenia, with linkage to many genes of small effect, maybe brought together via this "vitamin D hypothesis." We also discuss the possibility of a broader set of environmental and genetic factors interacting via the nuclear hormone receptors to affect the Development of the Brain leading to schizophrenia.

  • Vitamin D3-implications for Brain Development.
    The Journal of steroid biochemistry and molecular biology, 2004
    Co-Authors: John J. Mcgrath, Alan Mackay-sim, Thomas H. J. Burne, François P Féron, Darryl W. Eyles
    Abstract:

    There is growing evidence that 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) is active in the Brain but until recently there was a lack of evidence about its role during Brain Development. Guided by certain features of the epidemiology of schizophrenia, our group has explored the role of 1,25(OH)(2)D(3) in Brain Development using whole animal models and in vitro culture studies. The expression of the vitamin D receptor (VDR) in the embryonic rat Brain rises steadily between embryonic day 15-23, and 1,25(OH)(2)D(3) induces the expression of nerve growth factor and stimulates neurite outgrowth in embryonic hippocampal explant cultures. In the neonatal rat, low prenatal vitamin D(3) in utero leads to increased Brain size, altered Brain shape, enlarged ventricles, reduced expression of nerve growth factors, reduced expression of the low affinity p75 receptor and increased cellular proliferation. In summary, there is growing evidence that low prenatal levels of 1,25(OH)(2)D(3) can influence critical components of orderly Brain Development. It remains to be seen if these processes are of clinical relevance in humans, but in light of the high rates of hypovitaminosis D in pregnant women and neonates, this area warrants further scrutiny.

Darryl W. Eyles - One of the best experts on this subject based on the ideXlab platform.

  • Developmental vitamin D deficiency causes abnormal Brain Development.
    Psychoneuroendocrinology, 2009
    Co-Authors: Darryl W. Eyles, Francois Feron, John J. Mcgrath, X. Cui, J. P. Kesby, L. H. Harms, Thomas H. J. Burne
    Abstract:

    There is now clear evidence that vitamin D is involved in Brain Development. Our group is interested in environmental factors that shape Brain Development and how this may be relevant to neuropsychiatric diseases including schizophrenia. The origins of schizophrenia are considered Developmental. We hypothesised that Developmental vitamin D (DVD) deficiency may be the plausible neurobiological explanation for several important epidemiological correlates of schizophrenia namely: (1) the excess winter/spring birth rate, (2) increased incidence of the disease in 2nd generation Afro-Caribbean migrants and (3) increased urban birth rate. Moreover we have published two pieces of direct epidemiological support for this hypothesis in patients. In order to establish the "Biological Plausibility" of this hypothesis we have developed an animal model to study the effect of DVD deficiency on Brain Development. We do this by removing vitamin D from the diet of female rats prior to breeding. At birth we return all dams to a vitamin D containing diet. Using this procedure we impose a transient, gestational vitamin D deficiency, while maintaining normal calcium levels throughout. The Brains of offspring from DVD-deficient dams are characterised by (1) a mild distortion in Brain shape, (2) increased lateral ventricle volumes, (3) reduced differentiation and (4) diminished expression of neurotrophic factors. As adults, the alterations in ventricular volume persist and alterations in Brain gene and protein expression emerge. Adult DVD-deficient rats also display behavioural sensitivity to agents that induce psychosis (the NMDA antagonist MK-801) and have impairments in attentional processing. In this review we summarise the literature addressing the function of vitamin D on neuronal and non-neuronal cells as well as in vivo results from DVD-deficient animals. Our conclusions from these data are that vitamin D is a plausible biological risk factor for neuropsychiatric disorders and that vitamin D acts as a neurosteroid with direct effects on Brain Development.

  • Schizophrenia, vitamin D, and Brain Development.
    International review of neurobiology, 2004
    Co-Authors: Alan Mackay-sim, Francois Feron, Darryl W. Eyles, Thomas H. J. Burne, John J. Mcgrath
    Abstract:

    Schizophrenia research is invigorated at present by the recent discovery of several plausible candidate susceptibility genes identified from genetic linkage and gene expression studies of Brains from persons with schizophrenia. It is a current challenge to reconcile this gathering evidence for specific candidate susceptibility genes with the "neuroDevelopmental hypothesis," which posits that schizophrenia arises from gene-environment interactions that disrupt Brain Development. We make the case here that schizophrenia may result not from numerous genes of small effect, but a few genes of transcriptional regulation acting during Brain Development. In particular we propose that low vitamin D during Brain Development interacts with susceptibility genes to alter the trajectory of Brain Development, probably by epigenetic regulation that alters gene expression throughout adult life. Vitamin D is an attractive "environmental" candidate because it appears to explain several key epidemiological features of schizophrenia. Vitamin D is an attractive "genetic" candidate because its nuclear hormone receptor regulates gene expression and nervous system Development. The polygenic quality of schizophrenia, with linkage to many genes of small effect, maybe brought together via this "vitamin D hypothesis." We also discuss the possibility of a broader set of environmental and genetic factors interacting via the nuclear hormone receptors to affect the Development of the Brain leading to schizophrenia.

  • Vitamin D3-implications for Brain Development.
    The Journal of steroid biochemistry and molecular biology, 2004
    Co-Authors: John J. Mcgrath, Alan Mackay-sim, Thomas H. J. Burne, François P Féron, Darryl W. Eyles
    Abstract:

    There is growing evidence that 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) is active in the Brain but until recently there was a lack of evidence about its role during Brain Development. Guided by certain features of the epidemiology of schizophrenia, our group has explored the role of 1,25(OH)(2)D(3) in Brain Development using whole animal models and in vitro culture studies. The expression of the vitamin D receptor (VDR) in the embryonic rat Brain rises steadily between embryonic day 15-23, and 1,25(OH)(2)D(3) induces the expression of nerve growth factor and stimulates neurite outgrowth in embryonic hippocampal explant cultures. In the neonatal rat, low prenatal vitamin D(3) in utero leads to increased Brain size, altered Brain shape, enlarged ventricles, reduced expression of nerve growth factors, reduced expression of the low affinity p75 receptor and increased cellular proliferation. In summary, there is growing evidence that low prenatal levels of 1,25(OH)(2)D(3) can influence critical components of orderly Brain Development. It remains to be seen if these processes are of clinical relevance in humans, but in light of the high rates of hypovitaminosis D in pregnant women and neonates, this area warrants further scrutiny.

Joan Stiles - One of the best experts on this subject based on the ideXlab platform.

  • Principles of Brain Development.
    Wiley interdisciplinary reviews. Cognitive science, 2016
    Co-Authors: Joan Stiles
    Abstract:

    Throughout much of the 20th century, the major models of Brain Development were strongly deterministic. It was thought that Brain Development proceeds via a prescribed blueprint that is somehow innately specified in the organism. Contemporary models present a distinctly different view of both inheritance and Brain Development. First, we do not inherit blueprints or plans, we inherit genes and the cellular machinery for expressing them. Genes carry essential information for creating proteins, but do not determine biological processes or Developmental outcomes; the first cells contain the elements necessary for creating proteins based on the information coded in the nucleotide sequences of genes. Second, Brain Development is dynamic: the biological state of the Brain at any moment is the product of Developmental processes that involve an intricate interplay among genes and an ever-expanding range of environmental factors—from local cellular events to influences from the outside world. In science, models matter. They reflect underlying assumptions about how things can happen, and thus influence the kinds of questions we ask, the kinds of experiments we propose, the therapies we develop, and the educational curricula we construct. The dynamic model of Brain Development accounts for powerful neurobehavioral effects that can simply not be accommodated by deterministic models. WIREs Cogn Sci 2017, 8:e1402. doi: 10.1002/wcs.1402 For further resources related to this article, please visit the WIREs website.

  • Brain Development and the nature versus nurture debate.
    Progress in brain research, 2011
    Co-Authors: Joan Stiles
    Abstract:

    Over the past three decades, Developmental neurobiologists have made tremendous progress in defining basic principles of Brain Development. This work has changed the way we think about how Brains develop. Thirty years ago, the dominant model was strongly deterministic. The relationship between Brain and behavioral Development was viewed as unidirectional; that is, Brain maturation enables behavioral Development. The advent of modern neurobiological methods has provided overwhelming evidence that it is the interaction of genetic factors and the experience of the individual that guides and supports Brain Development. Brains do not develop normally in the absence of critical genetic signaling, and they do not develop normally in the absence of essential environmental input. The fundamental facts about Brain Development should be of critical importance to neuropsychologists trying to understand the relationship between Brain and behavioral Development. However, the underlying assumptions of most contemporary psychological models reflect largely outdated ideas about how the biological system develops and what it means for something to be innate. Thus, contemporary models of Brain Development challenge the foundational constructs of the nature versus nurture formulation in psychology. The key to understanding the origins and emergence of both the Brain and behavior lies in understanding how inherited and environmental factors are engaged in the dynamic and interactive processes that define and guide Development of the neurobehavioral system.

  • The basics of Brain Development
    Neuropsychology Review, 2010
    Co-Authors: Joan Stiles, Terry L. Jernigan
    Abstract:

    Over the past several decades, significant advances have been made in our understanding of the basic stages and mechanisms of mammalian Brain Development. Studies elucidating the neurobiology of Brain Development span the levels of neural organization from the macroanatomic, to the cellular, to the molecular. Together this large body of work provides a picture of Brain Development as the product of a complex series of dynamic and adaptive processes operating within a highly constrained, genetically organized but constantly changing context. The view of Brain Development that has emerged from the Developmental neurobiology literature presents both challenges and opportunities to psychologists seeking to understand the fundamental processes that underlie social and cognitive Development, and the neural systems that mediate them. This chapter is intended to provide an overview of some very basic principles of Brain Development, drawn from contemporary Developmental neurobiology, that may be of use to investigators from a wide range of disciplines.

Thomas H. J. Burne - One of the best experts on this subject based on the ideXlab platform.

  • Developmental vitamin D deficiency causes abnormal Brain Development.
    Psychoneuroendocrinology, 2009
    Co-Authors: Darryl W. Eyles, Francois Feron, John J. Mcgrath, X. Cui, J. P. Kesby, L. H. Harms, Thomas H. J. Burne
    Abstract:

    There is now clear evidence that vitamin D is involved in Brain Development. Our group is interested in environmental factors that shape Brain Development and how this may be relevant to neuropsychiatric diseases including schizophrenia. The origins of schizophrenia are considered Developmental. We hypothesised that Developmental vitamin D (DVD) deficiency may be the plausible neurobiological explanation for several important epidemiological correlates of schizophrenia namely: (1) the excess winter/spring birth rate, (2) increased incidence of the disease in 2nd generation Afro-Caribbean migrants and (3) increased urban birth rate. Moreover we have published two pieces of direct epidemiological support for this hypothesis in patients. In order to establish the "Biological Plausibility" of this hypothesis we have developed an animal model to study the effect of DVD deficiency on Brain Development. We do this by removing vitamin D from the diet of female rats prior to breeding. At birth we return all dams to a vitamin D containing diet. Using this procedure we impose a transient, gestational vitamin D deficiency, while maintaining normal calcium levels throughout. The Brains of offspring from DVD-deficient dams are characterised by (1) a mild distortion in Brain shape, (2) increased lateral ventricle volumes, (3) reduced differentiation and (4) diminished expression of neurotrophic factors. As adults, the alterations in ventricular volume persist and alterations in Brain gene and protein expression emerge. Adult DVD-deficient rats also display behavioural sensitivity to agents that induce psychosis (the NMDA antagonist MK-801) and have impairments in attentional processing. In this review we summarise the literature addressing the function of vitamin D on neuronal and non-neuronal cells as well as in vivo results from DVD-deficient animals. Our conclusions from these data are that vitamin D is a plausible biological risk factor for neuropsychiatric disorders and that vitamin D acts as a neurosteroid with direct effects on Brain Development.

  • Schizophrenia, vitamin D, and Brain Development.
    International review of neurobiology, 2004
    Co-Authors: Alan Mackay-sim, Francois Feron, Darryl W. Eyles, Thomas H. J. Burne, John J. Mcgrath
    Abstract:

    Schizophrenia research is invigorated at present by the recent discovery of several plausible candidate susceptibility genes identified from genetic linkage and gene expression studies of Brains from persons with schizophrenia. It is a current challenge to reconcile this gathering evidence for specific candidate susceptibility genes with the "neuroDevelopmental hypothesis," which posits that schizophrenia arises from gene-environment interactions that disrupt Brain Development. We make the case here that schizophrenia may result not from numerous genes of small effect, but a few genes of transcriptional regulation acting during Brain Development. In particular we propose that low vitamin D during Brain Development interacts with susceptibility genes to alter the trajectory of Brain Development, probably by epigenetic regulation that alters gene expression throughout adult life. Vitamin D is an attractive "environmental" candidate because it appears to explain several key epidemiological features of schizophrenia. Vitamin D is an attractive "genetic" candidate because its nuclear hormone receptor regulates gene expression and nervous system Development. The polygenic quality of schizophrenia, with linkage to many genes of small effect, maybe brought together via this "vitamin D hypothesis." We also discuss the possibility of a broader set of environmental and genetic factors interacting via the nuclear hormone receptors to affect the Development of the Brain leading to schizophrenia.

  • Vitamin D3-implications for Brain Development.
    The Journal of steroid biochemistry and molecular biology, 2004
    Co-Authors: John J. Mcgrath, Alan Mackay-sim, Thomas H. J. Burne, François P Féron, Darryl W. Eyles
    Abstract:

    There is growing evidence that 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) is active in the Brain but until recently there was a lack of evidence about its role during Brain Development. Guided by certain features of the epidemiology of schizophrenia, our group has explored the role of 1,25(OH)(2)D(3) in Brain Development using whole animal models and in vitro culture studies. The expression of the vitamin D receptor (VDR) in the embryonic rat Brain rises steadily between embryonic day 15-23, and 1,25(OH)(2)D(3) induces the expression of nerve growth factor and stimulates neurite outgrowth in embryonic hippocampal explant cultures. In the neonatal rat, low prenatal vitamin D(3) in utero leads to increased Brain size, altered Brain shape, enlarged ventricles, reduced expression of nerve growth factors, reduced expression of the low affinity p75 receptor and increased cellular proliferation. In summary, there is growing evidence that low prenatal levels of 1,25(OH)(2)D(3) can influence critical components of orderly Brain Development. It remains to be seen if these processes are of clinical relevance in humans, but in light of the high rates of hypovitaminosis D in pregnant women and neonates, this area warrants further scrutiny.

Nicholas Spitzer - One of the best experts on this subject based on the ideXlab platform.