Journal
NATURE REVIEWS NEUROSCIENCE
Volume 9, Issue 1, Pages 46-57Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrn2297
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Funding
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK064862] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH079829, R01MH051569, R01MH069148, R01MH071349] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG023580, R01AG029573] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [R21DA024443] Funding Source: NIH RePORTER
- NIA NIH HHS [R01 AG023580, R01 AG 029573, R01 AG 023580, AG 0616710, R01 AG029573] Funding Source: Medline
- NIDA NIH HHS [R21 DA 024443, R21 DA024443] Funding Source: Medline
- NIDDK NIH HHS [R01 DK 064862, R01 DK064862] Funding Source: Medline
- NIMH NIH HHS [R01 MH 51569, R01 MH071349, MH 069148, R01 MH 71349, R01 MH 079829, R01 MH071349-03, R01 MH069148, R01 MH079829, R01 MH051569, R01 MH079829-03] Funding Source: Medline
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In response to a peripheral infection, innate immune cells produce pro-inflammatory cytokines that act on the brain to cause sickness behaviour. When activation of the peripheral immune system continues unabated, such as during systemic infections, cancer or autoimmune diseases, the ensuing immune signalling to the brain can lead to an exacerbation of sickness and the development of symptoms of depression in vulnerable individuals. These phenomena might account for the increased prevalence of clinical depression in physically ill people. Inflammation is therefore an important biological event that might increase the risk of major depressive episodes, much like the more traditional psychosocial factors.
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