Peripheral markers of inflammation, oxidative

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whether we deal with depression only or with accompanying and broadly understood ... Biol. Psychiatry. http://dx.doi.org/10.1016/j.pnpbp.2017.05.023. (Epub.
Progress in Neuropsychopharmacology & Biological Psychiatry 80 (2018) 167

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Peripheral markers of inflammation, oxidative and nitrosative stress pathways and memory functions as a new target of pharmacotherapy in depression

MARK

Depression is a disease in which we observe constant mobilisation of the immune system regarding both the peripheral and central nervous system. An increase in the parameters of an active inflammatory process, including proinflammatory cytokines such as interleukins, TNF-α or interferon gamma, is noticeable in the patients with symptoms of depression. We can consider depression to be a chronic cold of the organism, which develops in response to the action of greater or smaller stressors accompanying us every day. Hyperactivity of the hypothalamic–pituitary–adrenal axis (HPA axis) and activation of the immune system are the source of irregularities in the activity of the kynurenine pathway. Its basic role in a healthy organism is to transform tryptophan into two essential compounds engaged in mood regulation, i.e. serotonin and melatonin. As a consequence of unfavourable metabolic processes, tryptophan leads to the formation of kynurenine (KYN), instead of serotonin and melatonin; kynurenine is a neurotoxic substrate which increases the risk of neurodegenerative and neurotoxic processes. This way, an active inflammatory process reduces the amount of tryptophan available to produce serotonin, which leads to the occurrence of symptoms of depression at a later stage. Both depression and a series of civilisation diseases (hypertension, coronary artery disease, diabetes, and even dementia) have the same immunologic background. An increase in the activity of the immune system and the unfavourable metabolic conversions described above are observed in each of the diseases mentioned. In case of each episode of depression, even a mild one, the efficiency of cognitive functions is reduced. This phenomenon is observed in our patients regardless of whether we deal with depression only or with accompanying and broadly understood somatic comorbidity as well. It is still undecided how depression should be treated. It seems that anti-inflammatory products should be the future in the therapy of depressive disorders and civilisation diseases. Not only is depression a significant clinical problem, but also a social and economic one. Approximately 800 billion euros are spent in Europe each year on the fight with the consequences of brain diseases. Among these diseases, more than 60% of social and economic costs are generated by mental disorders – mainly depressive disorders. Depression will have been the most frequent cause of incapacity for work in the general population by 2030. I have decided to dedicate this special edition of Progress in NeuroPsychopharmacology and Biological Psychiatry to this specific matter. Kanchanatawan et al. (2017), Czarny et al. (2017), Mossakowska-Wójcik et al. (2017), Gałecki and Talarowska (2017), Curzytek et al. (2017), Chang et al. (2017 May 20), and Chaves Filho et al. (2017) write about a new approach to the aetiology of depression in this edition. Therapeutic applications in case of symptoms of depression are described in the articles by Gałecki et al. (2017), Grygier et al. (2017), Brown et al. (2017), and Kim et al. (2017). The remaining articles are dedicated to neurodegenerative processes during an episode of depression.

References Brown, G.M., McIntyre, R.S., Rosenblat, J., Hardeland, R., 2017. Depressive disorders: processes leading to neurogeneration and potential novel treatments. Prog. Neuropsychopharmacol. Biol. Psychiatry. http://dx.doi.org/10.1016/j.pnpbp.2017.04.023. (Epub ahead of print). Chang, J.P., Lin, C.Y., Lin, P.Y., Shih, Y.H., Chiu, T.H., Ho, M., Yang, H.T., Huang, S.Y., Gałecki, P., Su, K.P., 2017. Polyunsaturated fatty acids and inflammatory markers in major depressive episodes during pregnancy. Prog. Neuropsychopharmacol. Biol. Psychiatry. http://dx.doi.org/10.1016/j.pnpbp.2017.05.008. (Epub ahead of print). Chaves Filho, A.J.M., Lima, C.N.C., Vasconcelos, S.M.M., de Lucena, D.F., Maes, M., Macedo, D., 2017. IDO chronic immune activation and tryptophan metabolic pathway: a potential pathophysiological link between depression and obesity. Prog. Neuropsychopharmacol. Biol. Psychiatry. http://dx.doi.org/10.1016/j.pnpbp.2017.04.035. (Epub ahead of print). Curzytek, K., Kubera, M., Trojan, E., Wójcik, K., Basta-Kaim, A., Detka, J., Maes, M., Rygula, R., 2017. The effects of pessimism on cell-mediated immunity in rats. Prog. Neuropsychopharmacol. Biol. Psychiatry. http://dx.doi.org/10.1016/j.pnpbp.2017.04.034. (Epub ahead of print). Czarny, P., Wigner, P., Galecki, P., Sliwinski, T., 2017. The interplay between inflammation, oxidative stress, DNA damage, DNA repair and mitochondrial dysfunction in depression. Prog. Neuropsychopharmacol. Biol. Psychiatry. http://dx.doi.org/10.1016/j.pnpbp.2017.06.036. (Epub ahead of print). Gałecki, P., Talarowska, M., 2017. Neurodevelopmental theory of depression. Prog. Neuropsychopharmacol. Biol. Psychiatry. http://dx.doi.org/10.1016/j.pnpbp.2017.05.023. (Epub ahead of print) Review. Gałecki, P., Mossakowska-Wójcik, J., Talarowska, M., 2017. The anti-inflammatory mechanism of antidepressants – SSRIs, SNRIs. Prog. Neuropsychopharmacol. Biol. Psychiatry. http:// dx.doi.org/10.1016/j.pnpbp.2017.03.016. (Epub ahead of print) Review. Grygier, B., Kubera, M., Wrona, D., Roman, A., Basta-Kaim, A., Gruca, P., Papp, M., Rogoz, Z., Leskiewicz, M., Budziszewska, B., Regulska, M., Korzeniak, B., Curzytek, K., Glombik, K., Slusarczyk, J., Maes, M., Lason, W., 2017. Stimulatory effect of desipramine on lung metastases of adenocarcinoma MADB 106 in stress highly-sensitive and stress non-reactive rats. Prog. Neuropsychopharmacol. Biol. Psychiatry. http://dx.doi.org/10.1016/j.pnpbp.2017.04.024. (Epub ahead of print). Kanchanatawan, B., Sirivichayakul, S., Carvalho, A.F., Anderson, G., Galecki, P., Maes, M., 2017. Depressive, anxiety and hypomanic symptoms in schizophrenia may be driven by tryptophan catabolite (TRYCAT) patterning of IgA and IgM responses directed to TRYCATs. Prog. Neuropsychopharmacol. Biol. Psychiatry. http://dx.doi.org/10.1016/j.pnpbp.2017. 06.033. (Epub ahead of print). Kim, S.W., Kang, H.J., Bae, K.Y., Shin, I.S., Hong, Y.J., Ahn, Y.K., Jeong, M.H., Berk, M., Yoon, J.S., Kim, J.M., 2017. Interactions between pro-inflammatory cytokines and statins on depression in patients with acute coronary syndrome. Prog. Neuropsychopharmacol. Biol. Psychiatry. http://dx.doi.org/10.1016/j.pnpbp.2017.07.003. (Epub ahead of print). Mossakowska-Wójcik, J., Orzechowska, A., Talarowska, M., Szemraj, J., Gałecki, P., 2017. The importance of TCF4 gene in the etiology of recurrent depressive disorders. Prog. Neuropsychopharmacol. Biol. Psychiatry. http://dx.doi.org/10.1016/j.pnpbp.2017.03.014. (Epub ahead of print).

Piotr Gałecki Department of Adult Psychiatry, Medical University of Lodz, Lodz, Poland E-mail address: [email protected] http://dx.doi.org/10.1016/j.pnpbp.2017.09.028

0278-5846/ © 2017 Published by Elsevier Inc.