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https://hdl.handle.net/2440/74497
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dc.contributor.author | Eyre, H. | - |
dc.contributor.author | Baune, B. | - |
dc.date.issued | 2012 | - |
dc.identifier.citation | Psychoneuroendocrinology, 2012; 37(9):1397-1416 | - |
dc.identifier.issn | 0306-4530 | - |
dc.identifier.issn | 1873-3360 | - |
dc.identifier.uri | http://hdl.handle.net/2440/74497 | - |
dc.description.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. | - |
dc.description.statementofresponsibility | Harris Eyre, Bernhard T. Baune | - |
dc.language.iso | en | - |
dc.publisher | Pergamon-Elsevier Science Ltd | - |
dc.rights | © 2012 Elsevier Ltd. All rights reserved. | - |
dc.source.uri | http://dx.doi.org/10.1016/j.psyneuen.2012.03.019 | - |
dc.subject | Neuroplasticity | - |
dc.subject | Depression | - |
dc.subject | Immune system | - |
dc.subject | Humoral | - |
dc.subject | Cellular | - |
dc.subject | Recovery | - |
dc.subject | Treatment | - |
dc.title | Neuroplastic changes in depression: A role for the immune system | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.1016/j.psyneuen.2012.03.019 | - |
pubs.publication-status | Published | - |
dc.identifier.orcid | Baune, B. [0000-0001-6548-426X] | - |
Appears in Collections: | Aurora harvest 4 Psychiatry publications |
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