Bücher von Yong-Ku Kim

This book reviews the relationship between cytokines, glia, and neurons in the pathophysiology of neuropsychiatric disorders and examines the mechanisms of action of the drugs used for the treatment of these disorders. Increasing evidence has suggested that glia perform important roles in various brain functions, but much remains to be learned about these crucial cells and their interplay with neurons. In addition, a better understanding of the interaction between inflammatory mediators, such as cytokines, and the activated immune response will be of critical importance for the development of new therapeutic strategies. These key areas are the focus of this book, which documents the latest research findings in the field. Evidence is provided for the role of inflammation-induced toxic metabolites from the tryptophan pathway in a wide range of neuropsychiatric disorders, including depression, schizophrenia, and Alzheimer's disease. In presenting state of the art knowledge on the interactions between cytokines, glia, and neurons, the book will help to pave the way for the development of novel targets for the prevention and treatment of neuropsychiatric disorders.

Major depressive disorder (MDD) is a complex and heterogeneous disorder, phenotypically and biologically. MDD may be caused by complex interaction between genes and environment in susceptible individuals. Thus, a combination of certain genetic polymorphism, environmental stress, and personal susceptibility ultimately may induce MDD. Gene-environment interactions in the pathophysiology of MDD lead to advancement in personalized medicine by means of genotyping for inter-individual variability in drug action and metabolism. Gene-environment interactions may explain why some subjects become depressed while others remain unaffected. The aim of this book is to describe current knowledge of MDD from the point of view of neurobiology, molecular genetics and cognition. The authors address a deep understanding of cognitive and neurobiological mechanisms involved in MDD.