Chronic Stress and Glucocorticoids: From Neuronal Plasticity to Neurodegeneration

Stress and stress hormones, glucocorticoids (GCs), exert widespread actions in central nervous system, ranging from the regulation of gene transcription, cellular signaling, modulation of synaptic structure, and transmission and glial function to behavior. Their actions are mediated by glucocorticoi...

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Published inJournal of neural transplantation & plasticity Vol. 2016; no. 2016; pp. 1 - 15
Main Authors Sotiropoulos, Ioannis, Almeida, Osborne F. X., Tronche, Francois, Silva, Joana Margarida, Rodrigues, Ana João, Vyas, Sheela, Sousa, Nuno
Format Journal Article
LanguageEnglish
Published Cairo, Egypt Hindawi Publishing Corporation 01.01.2016
John Wiley & Sons, Inc
Wiley
Subjects
Alzheimer Disease - etiology
Alzheimer Disease - metabolism
Alzheimer's disease
Animals
Brain - metabolism
Corticosteroids
Development and progression
DNA methylation
Epigenetics
Genes
Genetic aspects
Genetic transcription
Glucocorticoids - metabolism
Humans
Inflammation - complications
Inflammation - metabolism
Kinases
Life Sciences
Nervous system diseases
Neurobiology
Neurodegeneration
Neuronal Plasticity
Neurons
Neurons and Cognition
Neurophysiology
Neuroplasticity
Parkinson Disease - etiology
Parkinson Disease - metabolism
Parkinson's disease
Physiological aspects
Review
Risk Factors
Steroids
Stress, Psychological - complications
Stress, Psychological - metabolism
Online AccessGet full text

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Abstract Stress and stress hormones, glucocorticoids (GCs), exert widespread actions in central nervous system, ranging from the regulation of gene transcription, cellular signaling, modulation of synaptic structure, and transmission and glial function to behavior. Their actions are mediated by glucocorticoid and mineralocorticoid receptors which are nuclear receptors/transcription factors. While GCs primarily act to maintain homeostasis by inducing physiological and behavioral adaptation, prolonged exposure to stress and elevated GC levels may result in neuro- and psychopathology. There is now ample evidence for cause-effect relationships between prolonged stress, elevated GC levels, and cognitive and mood disorders while the evidence for a link between chronic stress/GC and neurodegenerative disorders such as Alzheimer’s (AD) and Parkinson’s (PD) diseases is growing. This brief review considers some of the cellular mechanisms through which stress and GC may contribute to the pathogenesis of AD and PD.
AbstractList Stress and stress hormones, glucocorticoids (GCs), exert widespread actions in central nervous system, ranging from the regulation of gene transcription, cellular signaling, modulation of synaptic structure, and transmission and glial function to behavior. Their actions are mediated by glucocorticoid and mineralocorticoid receptors which are nuclear receptors/transcription factors. While GCs primarily act to maintain homeostasis by inducing physiological and behavioral adaptation, prolonged exposure to stress and elevated GC levels may result in neuro- and psychopathology. There is now ample evidence for cause-effect relationships between prolonged stress, elevated GC levels, and cognitive and mood disorders while the evidence for a link between chronic stress/GC and neurodegenerative disorders such as Alzheimer’s (AD) and Parkinson’s (PD) diseases is growing. This brief review considers some of the cellular mechanisms through which stress and GC may contribute to the pathogenesis of AD and PD.
Stress and stress hormones, glucocorticoids (GCs), exert widespread actions in central nervous system, ranging from the regulation of gene transcription, cellular signaling, modulation of synaptic structure, and transmission and glial function to behavior. Their actions are mediated by glucocorticoid and mineralocorticoid receptors which are nuclear receptors/transcription factors. While GCs primarily act to maintain homeostasis by inducing physiological and behavioral adaptation, prolonged exposure to stress and elevated GC levels may result in neuro- and psychopathology. There is now ample evidence for cause-effect relationships between prolonged stress, elevated GC levels, and cognitive and mood disorders while the evidence for a link between chronic stress/GC and neurodegenerative disorders such as Alzheimer's (AD) and Parkinson's (PD) diseases is growing. This brief review considers some of the cellular mechanisms through which stress and GC may contribute to the pathogenesis of AD and PD.Stress and stress hormones, glucocorticoids (GCs), exert widespread actions in central nervous system, ranging from the regulation of gene transcription, cellular signaling, modulation of synaptic structure, and transmission and glial function to behavior. Their actions are mediated by glucocorticoid and mineralocorticoid receptors which are nuclear receptors/transcription factors. While GCs primarily act to maintain homeostasis by inducing physiological and behavioral adaptation, prolonged exposure to stress and elevated GC levels may result in neuro- and psychopathology. There is now ample evidence for cause-effect relationships between prolonged stress, elevated GC levels, and cognitive and mood disorders while the evidence for a link between chronic stress/GC and neurodegenerative disorders such as Alzheimer's (AD) and Parkinson's (PD) diseases is growing. This brief review considers some of the cellular mechanisms through which stress and GC may contribute to the pathogenesis of AD and PD.
Audience Academic
Author Sotiropoulos, Ioannis
Almeida, Osborne F. X.
Sousa, Nuno
Silva, Joana Margarida
Tronche, Francois
Rodrigues, Ana João
Vyas, Sheela
AuthorAffiliation 3 ICVS/3B's-PT Government Associate Laboratory, Guimarães, Braga, Portugal
1 Laboratory of Gene Regulation and Adaptive Behaviors, Department of Neuroscience Paris Seine, INSERM U1130, CNRS UMR 8246, Université Pierre et Marie Curie, Paris Cedex 05, France
4 Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, 80804 Munich, Germany
2 Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal
AuthorAffiliation_xml – name: 1 Laboratory of Gene Regulation and Adaptive Behaviors, Department of Neuroscience Paris Seine, INSERM U1130, CNRS UMR 8246, Université Pierre et Marie Curie, Paris Cedex 05, France
– name: 4 Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, 80804 Munich, Germany
– name: 3 ICVS/3B's-PT Government Associate Laboratory, Guimarães, Braga, Portugal
– name: 2 Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal
Author_xml – sequence: 1
  fullname: Sotiropoulos, Ioannis
– sequence: 2
  fullname: Almeida, Osborne F. X.
– sequence: 3
  fullname: Tronche, Francois
– sequence: 4
  fullname: Silva, Joana Margarida
– sequence: 5
  fullname: Rodrigues, Ana João
– sequence: 6
  fullname: Vyas, Sheela
– sequence: 7
  fullname: Sousa, Nuno
BackLink https://www.ncbi.nlm.nih.gov/pubmed/27034847$$D View this record in MEDLINE/PubMed
https://hal.sorbonne-universite.fr/hal-01310709$$DView record in HAL
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Snippet Stress and stress hormones, glucocorticoids (GCs), exert widespread actions in central nervous system, ranging from the regulation of gene transcription,...
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SubjectTerms Alzheimer Disease - etiology
Alzheimer Disease - metabolism
Alzheimer's disease
Animals
Brain - metabolism
Corticosteroids
Development and progression
DNA methylation
Epigenetics
Genes
Genetic aspects
Genetic transcription
Glucocorticoids - metabolism
Humans
Inflammation - complications
Inflammation - metabolism
Kinases
Life Sciences
Nervous system diseases
Neurobiology
Neurodegeneration
Neuronal Plasticity
Neurons
Neurons and Cognition
Neurophysiology
Neuroplasticity
Parkinson Disease - etiology
Parkinson Disease - metabolism
Parkinson's disease
Physiological aspects
Review
Risk Factors
Steroids
Stress, Psychological - complications
Stress, Psychological - metabolism
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Title Chronic Stress and Glucocorticoids: From Neuronal Plasticity to Neurodegeneration
URI https://search.emarefa.net/detail/BIM-1113222
https://dx.doi.org/10.1155/2016/6391686
https://www.ncbi.nlm.nih.gov/pubmed/27034847
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https://pubmed.ncbi.nlm.nih.gov/PMC4806285
https://doaj.org/article/52657507aaac4159993d284b934278b3
Volume 2016
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