oalib

Publish in OALib Journal

ISSN: 2333-9721

APC: Only $99

Submit

Any time

2019 ( 1 )

2018 ( 2 )

2016 ( 2 )

2015 ( 63 )

Custom range...

Search Results: 1 - 10 of 835 matches for " Shawn Hayley "
All listed articles are free for downloading (OA Articles)
Page 1 /835
Display every page Item
Toward an Anti-Inflammatory Strategy for Depression
Shawn Hayley
Frontiers in Behavioral Neuroscience , 2011, DOI: 10.3389/fnbeh.2011.00019
Abstract: It has become clear that the inflammatory immune system is altered during the course of clinical depression. In particular, studies on human patients have found depression to be associated with disturbances in the trafficking of cells of the adaptive immune system, coupled with elevations of innate immune messengers and pro-inflammatory cytokines. Paralleling these findings, stressor-based animal models of depression have implicated several cytokines, most notably interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α. Elevations of these cytokines and general inflammatory indicators, such as C-reactive protein, together with reductions of specific immune cells (e.g., T lymphocytes) might serve as useful biomarkers of depression or at least, certain subtypes of the disorder. Recent reports also suggest the possibility that anti-inflammatory agents could have therapeutic value in acting as adjunct treatments with traditional anti-depressants. Along these lines, we presently discuss the evidence for pro-inflammatory cytokine involvement in depression, as well as the possibility that anti-inflammatory agents and trophic cytokines themselves might have important anti-depressant properties.
Stressor-Like Effects of c-Jun N-Terminal Kinase (JNK) Inhibition
Melanie Clarke, Rowan Pentz, Jessica Bobyn, Shawn Hayley
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0044073
Abstract: There is an urgent need for novel treatment strategies for stressor related disorders, particularly depression and anxiety disorders. Indeed, existing drug treatments are only clinically successful in a subset of patients and relapse is common. This likely stems from the fact that stressor disorders are heterogeneous with multiple biological pathways being affected. To this end, the present investigation sought to assess in mice the contribution of the c-Jun N terminal kinase (JNK) pathway to the behavioral, hormonal and neurochemical effects of an acute stressor. Indeed, although JNK has been shown to modulate glucocorticoid receptors in vitro, virtually nothing is known of the role for JNK in affecting stressor induced pathology. We presently found that the JNK antagonist, SP600125, (but not the p38 antagonist, SB203580) increased plasma corticosterone levels under resting conditions and in the context of an acute stressor (wet bedding + restraint). SP600125 also reduced exploration in an open field arena, but prevented the stressor induced increase in open arm exploration in an elevated plus maze. Finally, SP600125 affected noradrenergic activity in the central amygdala and locus coruleus under resting condition, but prevented the noradrenergic effects within the paraventricular nucleus of the hypothalamus that were induced by the acute stressor exposure. These data suggest inhibiting endogenous JNK can have stressor-like corticoid, behavioral and central monoamine effects under basal conditions, but can actually reverse some behavioral and neurochemical effects of an acute stressor. Thus, endogenous JNK appears to affect stress relevant processes in a context-dependent manner.
Proinflammatory cytokines differentially influence adult hippocampal cell proliferation depending upon the route and chronicity of administration
Julie Anne Seguin, Jordan Brennan, Emily Mangano, Shawn Hayley
Neuropsychiatric Disease and Treatment , 2009, DOI: http://dx.doi.org/10.2147/NDT.S4476
Abstract: oinflammatory cytokines differentially influence adult hippocampal cell proliferation depending upon the route and chronicity of administration Original Research (4343) Total Article Views Authors: Julie Anne Seguin, Jordan Brennan, Emily Mangano, Shawn Hayley Published Date December 2008 Volume 2009:5 Pages 5 - 14 DOI: http://dx.doi.org/10.2147/NDT.S4476 Julie Anne Seguin, Jordan Brennan, Emily Mangano, Shawn Hayley Institute of Neuroscience, Carleton University, Ottawa, Ontario, Canada Abstract: Disturbances of hippocampal plasticity, including impaired dendritic branching and reductions of neurogenesis, are provoked by stressful insults and may occur in depression. Although corticoids likely contribute to stressor-induced reductions of neurogenesis, other signaling messengers, including pro-inflammatory cytokines might also be involved. Accordingly, the present investigation assessed whether three proinflammatory cytokines, namely interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) (associated with depression) influenced cellular proliferation within the hippocampus. In this regard, systemic administration of TNF-α reduced 5-bromo-2-deoxyuridine (BrdU) labeling within the hippocampus, whereas IL-1β and IL-6 had no such effect. However, repeated but not a single intra-hippocampal infusion of IL-6 and IL-1β actually increased cellular proliferation and IL-6 infusion also enhanced microglial staining within the hippocampus. Yet, no changes in doublecortin expression were apparent, suggesting that the cytokine did not influence the birth of cells destined to become neurons. Essentially, the route of administration and chronicity of cytokine administration had a marked influence upon the nature of hippocampal alterations provoked, suggesting that cytokines may differentially regulate hippocampal plasticity in neuropsychiatric conditions.
Proinflammatory cytokines differentially influence adult hippocampal cell proliferation depending upon the route and chronicity of administration
Julie Anne Seguin,Jordan Brennan,Emily Mangano,Shawn Hayley
Neuropsychiatric Disease and Treatment , 2008,
Abstract: Julie Anne Seguin, Jordan Brennan, Emily Mangano, Shawn HayleyInstitute of Neuroscience, Carleton University, Ottawa, Ontario, CanadaAbstract: Disturbances of hippocampal plasticity, including impaired dendritic branching and reductions of neurogenesis, are provoked by stressful insults and may occur in depression. Although corticoids likely contribute to stressor-induced reductions of neurogenesis, other signaling messengers, including pro-inflammatory cytokines might also be involved. Accordingly, the present investigation assessed whether three proinflammatory cytokines, namely interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) (associated with depression) influenced cellular proliferation within the hippocampus. In this regard, systemic administration of TNF-α reduced 5-bromo-2-deoxyuridine (BrdU) labeling within the hippocampus, whereas IL-1β and IL-6 had no such effect. However, repeated but not a single intra-hippocampal infusion of IL-6 and IL-1β actually increased cellular proliferation and IL-6 infusion also enhanced microglial staining within the hippocampus. Yet, no changes in doublecortin expression were apparent, suggesting that the cytokine did not influence the birth of cells destined to become neurons. Essentially, the route of administration and chronicity of cytokine administration had a marked influence upon the nature of hippocampal alterations provoked, suggesting that cytokines may differentially regulate hippocampal plasticity in neuropsychiatric conditions.Keywords: cytokine, depression, neuroplasticity, hippocampus, stressor
Inflammatory Mechanisms of Neurodegeneration in Toxin-Based Models of Parkinson's Disease
Darcy Litteljohn,Emily Mangano,Melanie Clarke,Jessica Bobyn,Kerry Moloney,Shawn Hayley
Parkinson's Disease , 2011, DOI: 10.4061/2011/713517
Abstract: Parkinson's disease (PD) has been associated with exposure to a variety of environmental agents, including pesticides, heavy metals, and organic pollutants; and inflammatory processes appear to constitute a common mechanistic link among these insults. Indeed, toxin exposure has been repeatedly demonstrated to induce the release of oxidative and inflammatory factors from immunocompetent microglia, leading to damage and death of midbrain dopamine (DA) neurons. In particular, proinflammatory cytokines such as tumor necrosis factor- and interferon- , which are produced locally within the brain by microglia, have been implicated in the loss of DA neurons in toxin-based models of PD; and mounting evidence suggests a contributory role of the inflammatory enzyme, cyclooxygenase-2. Likewise, immune-activating bacterial and viral agents were reported to have neurodegenerative effects themselves and to augment the deleterious impact of chemical toxins upon DA neurons. The present paper will focus upon the evidence linking microglia and their inflammatory processes to the death of DA neurons following toxin exposure. Particular attention will be devoted to the possibility that environmental toxins can activate microglia, resulting in these cells adopting a “sensitized” state that favors the production of proinflammatory cytokines and damaging oxidative radicals. 1. Introduction Parkinson’s disease (PD) is the most common neurodegenerative disorder of motor functioning, affecting nearly six million people worldwide. The disorder is particularly prevalent in the elderly population, with a typical clinical onset after 60?65 years of age. Notwithstanding the rare familial forms of PD that appear to have a strong genetic component, the vast majority of PD cases (upwards of 90%) are idiopathic in nature. Regardless of etiology, PD is characterized primarily by the progressive degeneration of dopamine (DA) neurons within the substantia nigra pars compacta (SNc) region of the midbrain, resulting in the diminished monoamine release at downstream striatal nerve terminals. Clinically, the Parkinsonian syndrome, which typically becomes manifest following 50?60% SNc DA neuron loss, comprises a constellation of well-defined motor symptoms, including bradykinesia, hypokinesia (or akinesia), cogwheel rigidity, resting tremor, and postural instability [1]. In addition to the motor impairment evident in all PD cases, a substantial number of PD patients also display prominent “nonmotor” symptoms (many of which manifest before the onset of motor decline and PD diagnosis), including
An in vivo animal study assessing long-term changes in hypothalamic cytokines following perinatal exposure to a chemical mixture based on Arctic maternal body burden
Shawn Hayley, Emily Mangano, Geoffrey Crowe, Nanqin Li, Wayne J Bowers
Environmental Health , 2011, DOI: 10.1186/1476-069x-10-65
Abstract: Rats were dosed during gestation and lactation and cytokine levels were measured in the brains of offspring at five months of age. Hypothalamic cytokine protein levels were measured with a suspension-based array system and differences were determined using ANOVA and post hoc statistical tests.The early life PCB treatment alone significantly elevated hypothalamic interleukin-6 (IL-6) levels in rats at five months of age to a degree comparable to that of the entire chemical mixture. Similarly, the full mixture (and to a lesser degree PCBs alone) elevated levels of the pro-inflammatory cytokine, IL-1b, as well as the anti-inflammatory cytokine, IL-10. The full mixture of chemicals also moderately increased (in an additive fashion) hypothalamic levels of the pro-inflammatory cytokines, IL-12 and tumor necrosis factor (TNF-α). Challenge with bacterial endotoxin at adulthood generally increased hypothalamic levels to such a degree that differences between the perinatally treated chemical groups were no longer detectable.These data suggest that exposure at critical neurodevelopmental times to environmental chemicals at concentrations and combinations reflective of those observed in vulnerable population can have enduring consequences upon cytokines that are thought to contribute to a range of pathological states. In particular, such protracted alterations in the cytokine balance within the hypothalamus would be expected to favor marked changes in neuro-immune and hormonal communication that could have profound behavioral consequences.A wide array of substances found in the environment, including metals (e.g. lead, iron, mercury), polychlorinated biphenyls (PCBs) and pesticides can be toxic to the central nervous system (CNS). Sensitive sub-populations, such as the developing fetus, as well as elderly individuals that are already at increased risk of illness may be especially vulnerable to the neurological effects of such toxins [1-4]. Indeed, considerable epidemiological e
Viral-toxin interactions and Parkinson’s disease: poly(I:C) priming enhanced the neurodegenerative effects of paraquat
Jessica Bobyn, Emily N Mangano, Anusha Gandhi, Eric Nelson, Kerry Moloney, Melanie Clarke, Shawn Hayley
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-86
Abstract: Mice received a supra-nigral infusion of 5 μg of the double-stranded RNA viral analog, polyinosinic: polycytidylic acid (poly(I:C)), followed 2, 7 or 14 days later by administration of the pesticide, paraquat (nine 10 mg/kg injections over three weeks).As hypothesized, poly(I:C) pre-treatment enhanced dopamine (DA) neuron loss in the substantia nigra pars compacta elicited by subsequent paraquat treatment. The augmented neuronal loss was accompanied by robust signs of microglial activation, and by increased expression of the catalytic subunit (gp91) of the NADPH oxidase oxidative stress enzyme. However, the paraquat and poly(I:C) treatments did not appreciably affect home-cage activity, striatal DA terminals, or subventricular neurogenesis.These findings suggest that viral agents can sensitize microglial-dependent inflammatory responses, thereby rendering nigral DA neurons vulnerable to further environmental toxin exposure.
Antidepressant-Like Effects of Erythropoietin: A Focus on Behavioural and Hippocampal Processes
Meagan Osborn, Nazneen Rustom, Melanie Clarke, Darcy Litteljohn, Chris Rudyk, Hymie Anisman, Shawn Hayley
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0072813
Abstract: Depression is a chronic and debilitating condition with a significant degree of relapse and treatment resistance that could stem, at least in part, from disturbances of neuroplasticity. This has led to an increased focus on treatment strategies that target brain derived neurotrophic factor (BDNF), synaptic plasticity and adult neurogenesis. In the current study we aimed to assess whether erythropoietin (EPO) would have antidepressant-like effects given its already established pro-trophic actions. In particular, we assessed whether EPO would diminish the deleterious effects of a social stressor in mice. Indeed, EPO induced anxiolytic and antidepressant-like responses in a forced swim test, open field, elevated-plus maze, and a novelty test, and appeared to blunt some of the negative behavioural effects of a social stressor. Furthermore, EPO promoted adult hippocampal neurogenesis, an important feature of effective antidepressants. Finally, a separate study using the mTOR inhibitor rapamycin revealed that antagonizing this pathway prevented the impact of EPO upon forced swim performance. These data are consistent with previous findings showing that the mTOR pathway and its neurogenic and synaptogenic effects might mediate the behavioral consequences of antidepressant agents. Our findings further highlight EPO as a possible adjunct treatment for affective disorders, as well as other stressor associated disorders of impaired neuroplasticity.
The Role of the Val66Met Polymorphism of the Brain Derived Neurotrophic Factor Gene in Coping Strategies Relevant to Depressive Symptoms
Warren Caldwell, Opal A. McInnis, Robyn J. McQuaid, Gele Liu, John D. Stead, Hymie Anisman, Shawn Hayley
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0065547
Abstract: Disturbances of brain derived neurotrophic factor (BDNF) signalling have been implicated in the evolution of depression, which likely arises, in part, as a result of diminished synaptic plasticity. Predictably, given stressor involvement in depression, BDNF is affected by recent stressors as well as stressors such as neglect experienced in early life. The effects of early life maltreatment in altering BDNF signalling may be particularly apparent among those individuals with specific BDNF polymorphisms. We examined whether polymorphisms of the Val66Met genotype might be influential in moderating how early-life events play out with respect to later coping styles, cognitive flexibility and depressive features. Among male and female undergraduate students (N = 124), childhood neglect was highly related to subsequent depressive symptoms. This outcome was moderated by the BDNF polymorphism in the sense that depressive symptoms appeared higher in Met carriers who reported low levels of neglect than in those with the Val/Val allele. However, under conditions of high neglect depressive symptoms only increased in the Val/Val individuals. In effect, the Met polymorphism was associated with depressive features, but did not interact with early life neglect in predicting later depressive features. It was further observed that among the Val/Val individuals, the relationship between neglect and depression was mediated by emotion-focused styles and diminished perceived control, whereas this mediation was not apparent in Met carriers. In contrast to the more typical view regarding this polymorphism, the data are consistent with the perspective that in the presence of synaptic plasticity presumably associated with the Val/Val genotype, neglect allows for the emergence of specific appraisal and coping styles, which are tied to depression. In the case of the reduced degree of neuroplasticity expected in the Met carriers, early life adverse experiences are not tied to coping styles, and hence less likely to be translated into depressive states.
The theory of Realistic Mathematics Education as a theoretical framework for teaching low attainers in mathematics
Hayley Barnes
Pythagoras , 2011, DOI: 10.4102/pythagoras.v33i3.120
Abstract: This article recounts the process embarked on and reasons for selecting the theory of Realistic Mathematics Education (RME) as the theoretical framework in a study carried out with low attaining learners. In the study an intervention for low attaining grade 8 mathematics learners was implemented in an attempt to improve the understanding of the participants with regard to place value, fractions and decimals, and to identify characteristics of this type of intervention and potential design principles that could be applied in similar interventions. In this article, the theoretical framework for the intervention is discussed and theoretical (rather than empirical) reasons for selecting the theory of Realistic Mathematics Education (RME) for use with low attainers are put forward. From a literature review that looked at the teaching and learning of mathematics to learners who fall into the category of performing below the required standard, five common aspects emerged. Once these aspects had been identified, a theory in mathematics education was sought that encompassed these five aspects. The theory of RME was subsequently selected as the theoretical framework to drive the design and implementation of the intervention and is being suggested as a possible way forward for working with low attaining learners.
Page 1 /835
Display every page Item


Home
Copyright © 2008-2017 Open Access Library. All rights reserved.