University of Adelaide Library

Adelaide Research and Scholarship : Schools and Disciplines : School of Medicine : Psychiatry : Psychiatry publications

Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/74497

Type: Journal article
Title: Neuroplastic changes in depression: A role for the immune system
Author: Eyre, H.
Baune, B.
Citation: PsychoNeuroendocrinology, 2012; 37(9):1397-1416
Publisher: Pergamon-Elsevier Science Ltd
Issue Date: 2012
ISSN: 0306-4530
1873-3360
Statement of
Responsibility: 
Harris Eyre, Bernhard T. Baune
Abstract: Accumulating evidence suggests that there is a rich cross-talk between the neuroimmune system and neuroplasticity mechanisms under both physiological conditions and pathophysiological conditions in depression. Anti-neuroplastic changes which occur in depression include a decrease in proliferation of neural stem cells (NSCs), decreased survival of neuroblasts and immature neurons, impaired neurocircuitry (cortical-striatal-limbic circuits), reduced levels of neurotrophins, reduced spine density and dendritic retraction. Since both humoral and cellular immune factors have been implicated in neuroplastic processes, in this review we present a model suggesting that neuroplastic processes in depression are mediated through various neuroimmune mechanisms. The review puts forward a model in that both humoral and cellular neuroimmune factors are involved with impairing neuroplasticity under pathophysiological conditions such as depression. Specifically, neuroimmune factors including interleukin (IL)-1, IL-6, tumour necrosis factor (TNF)-α, CD4⁺CD25⁺T regulatory cells (T reg), self-specific CD4⁺T cells, monocyte-derived macrophages, microglia and astrocytes are shown to be vital to processes of neuroplasticity such as long-term potentiation (LTP), NSC survival, synaptic branching, neurotrophin regulation and neurogenesis. In rodent models of depression, IL-1, IL-6 and TNF are associated with reduced hippocampal neurogenesis; mechanisms which are associated with this include the stress-activated protein kinase (SAPK)/Janus Kinase (JNK) pathway, hypoxia-inducible factors (HIF)-1α, JAK-Signal Transducer and Activator of Transcription (STAT) pathway, mitogen-activated protein kinase (MAPK)/cAMP responsive element binding protein (CREB) pathway, Ras-MAPK, PI-3 kinase, IKK/nuclear factor (NF)-κB and TGFβ activated kinase-1 (TAK-1). Neuroimmunological mechanisms have an active role in the neuroplastic changes associated with depression. Since therapies in depression, including antidepressants (AD), omega-3 polyunsaturated fatty acids (PUFAs) and physical activity exert neuroplasticity-enhancing effects potentially mediated by neuroimmune mechanisms, the immune system might serve as a promising target for interventions in depression.
Keywords: Neuroplasticity; Depression; Immune system; Humoral; Cellular; Recovery; Treatment
Rights: © 2012 Elsevier Ltd. All rights reserved.
RMID: 0020122594
DOI: 10.1016/j.psyneuen.2012.03.019
Appears in Collections:Psychiatry publications
View citing articles in: Web of Science
Google Scholar
Scopus

There are no files associated with this item.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

 

© 2008 The University of Adelaide
library@adelaide.edu.au
CRICOS Provider Number 00123M
Service Charter | Copyright | Privacy | Disclaimer