[Immune-inflammatory and autoimmune mechanisms in postpartum depression].

Postpartum depression is a debilitating mental disorder with a high prevalence, usually related with a past psychiatric history of major depressive disorder, postpartum depression, bipolar disorder, premenstrual syndrome (PMS), and perinatal depressive symptoms during gestation. However, the existing literature does not sufficiently elucidate the pathophysiology of this clinical entity which appears in such a crucial period of woman's life. This review aims to search the available data regarding the involvement of immunological and autoimmune mechanisms in its onset. A literature review was conducted using web-based search engines provided by PubMed (for Medline database) and Google Scholar. Manuscripts in English and Greek language were included for the period 19902017. Nowadays, a large body of evidence indicates that depressive disorders are accompanied by activated neuro-immune, neuro-oxidative and neuro-nitrosative stress (IO&NS) pathways. However, clinical research regarding the biological mechanisms associated with PPD is a tough challenge as pregnancy and puerperium are periods of adaptive changes in pregnant women by definition. Two of the systems that have been studied as potentially contributing to the onset of PPD are: the activation of the Inflammatory Response System (IRS) and the deregulation of the Hypothalamic-PituitaryAdrenal axis (HPA). Controversial data indicate dysregulation of cytokines and other inflammatory agents in patients with PPD, as well as, a close correlation of immune-inflammatory mechanisms and kynurenine pathway. PPD has been closely associated with autoimmune diseases. It is notable that this entity shares many common traits with autoimmune diseases such as the genetic susceptibility, family history, the high correlation with other autoimmune diseases, clinical exacerbations and remissions, women's superiority in prevalence, and the possible re-occurrence during a future pregnancy. These facts suggest that the typical postpartum flare pattern, and other clinical characteristics, point towards an autoimmune etiology for PPD. There are indications that immune-inflammatory and autoimmune mechanisms may be the key to deciphering the complex pathophysiological pathways associated with the onset of PPD. Clinical studies have been insufficient to make clear the causative correlations of the underlying mechanisms involved. Future research could focus on the immune-inflammatory processes associated with the onset of the disease, as well as on potential biomarkers for an early diagnosis and an effective treatment of PPD.

[Kynurenine pathway in bipolar disorder].

Bipolar disorder (BD) is a chronic psychiatric illness which, among other things, is characterized by cerebral dysfunctions, cognitive disorders and sleep disturbances. The neurobiological basis of these processes remains unclear. In recent years, studies have focused on the role of immune-inflammatory mechanisms induced by the tryptophan metabolism pathway (TRP) and the kynurenine pathway (KYN). Emerging data correlates TRP and KYN metabolites with BD's pathophysiology and course. The purpose of this review is to search the available data on the involvement of KYN's pathway in the pathophysiology, the clinical presentation and the course of BD. A systematic literature review was conducted using web-based search engines provided by PubMed (for Medline database) and Google Scholar. The search languages were English and Greek and the entries Key phrases used for the research were: bipolar disorder, depression, mania, tryptophan, kynurenine pathway, cognitive dysfunction, sleep disorder, neuroimmunology, neuroinflammation manuscripts written or published in English and Greek language. The KYN pathway is actively involved in the pathophysiology of BD. The increase in neurotoxic weight of the neuroprotective derivatives of the pathway is associated with cognitive impairment that accompany the clinical presentation of the disease. In addition, some of these metabolites are also suspected of sleep disorders in BD. Further studies are needed to investigate the mechanisms involved. The KYN pathway is a highly interesting field of encounter and interaction of the immune inflammatory system with the CNS, both involved in the pathophysiology of BD in a variety of ways. Future research can focus on clarifying the role of the metabolites of this pathway, potentially highlighting new therapeutic goals. Additionally, consideration could be given to approaching the metabolites of the KYN pathway as biomarkers for early detection, staging and monitoring of BD patients.