@misc{oai:kawasakigakuen.repo.nii.ac.jp:00000316,
 author = {Katsuhiko YAMASAKI and Masatoshi TAKEDA},
 month = {Dec},
 note = {Major depressive disorder (MDD) is a leading cause of disability. It is associated with the highest disability-adjusted life year (DALY) value among all diseases and disorders, placing a significant burden on society. Thus, new advances in treatment methods based on the pathogenesis of MDD are strongly required. Historically, the monoamine hypothesis has been the major theory of depression, but it is too simplistic. It cannot explain the latency of response in the therapeutic action of antidepressants, and up to 30% of depressed patients fail to achieve remission despite multiple treatment trials. Over the past three decades, research has suggested that inflammatory processes are involved in the onset and maintenance of MDD; the inflammatory hypothesis has been proposed. This review will highlight the association between inflammation and the nervous system and the role of inflammation in the pathogenesis of MDD, including whether chronic stress (e.g., psychosocial stress) activates the inflammatory response, what kind of upstream neurogenic processes translate physiologic stress into inflammatory responses, communication pathways, or mechanisms by which the peripheral immune system can influence the brain and behavior; and the pathophysiology by which inflammation affects the nervous system and leads to MDD. Once cytokine signals reach the brain, they can interact with every pathophysiologic domain relevant to mood regulation, which includes neurotransmitter function, hypothalamic-pituitary-adrenal (HPA) axis activity, neural plasticity, and alteration of brain circuitry. Recent data demonstrating the importance of cytokines as biomarkers will also be presented., Review Article},
 title = {Pathophysiology of major depressive disorder related to the relationship between inflammation and the nervous system},
 year = {2020}
}