Chronic Stress and Glucocorticoids: From Neuronal Plasticity to Neurodegeneration

Author:

Vyas Sheela1,Rodrigues Ana João23,Silva Joana Margarida23,Tronche Francois1,Almeida Osborne F. X.4,Sousa Nuno23,Sotiropoulos Ioannis23

Affiliation:

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

2. Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal

3. ICVS/3B’s-PT Government Associate Laboratory, Guimarães, Braga, Portugal

4. Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, 80804 Munich, Germany

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.

Funder

Fundação para a Ciência e a Tecnologia

Publisher

Hindawi Limited

Subject

Clinical Neurology,Neurology

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