de Beaurepaire Renaud
CH Paul Guiraud, 54, avenue de la République, 94806 Villejuif, France.
Brain Behav Immun. 2002 Oct;16(5):610-7. doi: 10.1016/s0889-1591(02)00005-3.
The cytokine hypothesis of depression raises a certain number of questions. These questions include: the inability of the theory to account for the classical (Freudian) psychodynamics of depression; the role of sensitization in cytokine-induced depression; the compatibility of some of the effects of cytokines (on sleep, on cognition, on the HPA) with the hypothesis; the possibility of occurrence of depression in the absence of an increase in circulating cytokines; the nature of the relationships between cytokines, stress, and depression; the compatibility of the effects of cytokines on brain monoamines with the current monoamine hypothesis of depression; the inability of antidepressants to fully abrogate the brain effects of individual cytokines in animal experiments. Based on these limitations of the theory, it is proposed to define a new clinical entity designated as "the cytokine-associated depressive syndrome."
抑郁症的细胞因子假说引发了一些问题。这些问题包括：该理论无法解释抑郁症的经典（弗洛伊德式）心理动力学；致敏作用在细胞因子诱导的抑郁症中的作用；细胞因子的某些作用（对睡眠、认知、下丘脑-垂体-肾上腺轴的作用）与该假说的兼容性；在循环细胞因子未增加的情况下发生抑郁症的可能性；细胞因子、应激和抑郁症之间关系的本质；细胞因子对脑单胺类物质的作用与当前抑郁症单胺假说的兼容性；在动物实验中抗抑郁药无法完全消除单个细胞因子对大脑的影响。基于该理论的这些局限性，有人提议定义一种新的临床实体，称为“细胞因子相关抑郁综合征”。
