Depression's multiple comorbidities explained by (neuro)inflammatory and oxidative & nitrosative stress pathways

Maes, Michael, Kubera, Marta, Obuchowiczwa, Ewa, Goehler, Lisa and Brzeszcz, Joanna 2011, Depression's multiple comorbidities explained by (neuro)inflammatory and oxidative & nitrosative stress pathways, Neuroendocrinology letters, vol. 32, no. 1, pp. 7-24.

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Title Depression's multiple comorbidities explained by (neuro)inflammatory and oxidative & nitrosative stress pathways
Author(s) Maes, Michael
Kubera, Marta
Obuchowiczwa, Ewa
Goehler, Lisa
Brzeszcz, Joanna
Journal name Neuroendocrinology letters
Volume number 32
Issue number 1
Start page 7
End page 24
Total pages 18
Publisher Maghira & Maas Publications
Place of publication Stockholm, Sweden
Publication date 2011
ISSN 0172-780X
Keyword(s) depression
oxidative stress
medical illness
Summary There is now evidence that depression, as characterized by melancholic symptoms, anxiety, and fatigue and somatic (F&S) symptoms, is the clinical expression of peripheral cell-mediated activation, inflammation and induction of oxidative and nitrosative stress (IO&NS) pathways and of central microglial activation, decreased neurogenesis and increased apoptosis. This review gives an explanation for the multiple “co-morbidities” between depression and a large variety of a) brain disorders related to neurodegeneration, e.g. Alzheimer’s, Parkinson’s and Huntington’s disease, multiple sclerosis and stroke; b) medical disorders, such as cardiovascular disorder, chronic fatigue syndrome, chronic obstructive pulmonary disease, rheumatoid arthritis, psoriasis, systemic lupus erythematosus, inflammatory bowel disease, irritable bowel syndrome, leaky gut, diabetes type 1 and 2, obesity and the metabolic syndrome, and HIV infection; and c) conditions, such as hemodialysis, interferon-α-based immunotherapy, the postnatal period and psychosocial stressors. The common denominator of all those disorders/conditions is the presence of microglial activation and/or activation of peripheral IO&NS pathways. There is evidence that shared peripheral and / or central IO&NS pathways underpin the pathophysiology of depression and the previously mentioned disorders and that activation of these IO&NS pathways contributes to shared risk. The IO&NS pathways function as a smoke sensor that detect threats in the peripheral and central parts of the body and signal these threats as melancholic, anxiety, and fatigue and somatic (F&S) symptoms. The presence of concomitant depression is strongly associated with a lower quality of life and increased morbidity and mortality in medical disorders. This may be explained since depression contributes to increased (neuro)inflammatory burden and may therefore drive the inflammatory and degenerative progression. It is concluded that the activation of peripheral and / or central IO&NS pathways may explain the co-occurrence of depression with the above disorders. This shows that depression belongs to the spectrum of inflammatory and degenerative disorders.
Language eng
Field of Research 119999 Medical and Health Sciences not elsewhere classified
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2011, Neuroendocrinology Letters
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