Konstantinou Ger, Papageorgiou C C, Angelopoulos E
Department of Psychiatry, 251 Hellenic Airforce V.A. General Hospital.
1st Department of Psychiatry, Medical School, National and Kapodistrian University of Athens, Eginition Hospital, Athens, Greece.
Psychiatriki. 2018 Oct-Dec;29(4):338-348. doi: 10.22365/jpsych.2018.294.338.
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.
双相情感障碍（BD）是一种慢性精神疾病，其特征包括大脑功能障碍、认知障碍和睡眠障碍等。这些过程的神经生物学基础仍不清楚。近年来，研究聚焦于色氨酸代谢途径（TRP）和犬尿氨酸途径（KYN）诱导的免疫炎症机制的作用。新出现的数据将TRP和KYN代谢物与BD的病理生理学及病程联系起来。本综述的目的是搜索有关KYN途径参与BD病理生理学、临床表现及病程的现有数据。使用PubMed（用于Medline数据库）和谷歌学术提供的基于网络的搜索引擎进行了系统的文献综述。搜索语言为英语和希腊语，用于研究的关键词组包括：双相情感障碍、抑郁、躁狂、色氨酸、犬尿氨酸途径、认知功能障碍、睡眠障碍、神经免疫学、神经炎症，以英语和希腊语撰写或发表的手稿。KYN途径积极参与BD的病理生理学过程。该途径神经保护衍生物的神经毒性重量增加与该疾病临床表现伴随的认知障碍相关。此外，这些代谢物中的一些还被怀疑与BD的睡眠障碍有关。需要进一步研究以调查其中涉及的机制。KYN途径是免疫炎症系统与中枢神经系统相遇和相互作用的一个非常有趣的领域，两者都以多种方式参与BD的病理生理学过程。未来的研究可以集中在阐明该途径代谢物的作用上，这可能会突出新的治疗靶点。此外，可以考虑将KYN途径的代谢物作为BD患者早期检测、分期和监测的生物标志物。
