Neuroimmune-endocrine crosstalk in schizophrenia and mood disorders.
Neuroimmune-endocrine crosstalk in schizophrenia and mood disorders.
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DOI：
10.1586/14737175.6.7.1017
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发表时间：
2006-07-01
影响因子：
4.3
通讯作者：
Schwarz, Markus J
中科院分区：
文献类型：
--
作者：
Muller, Norbert;Schwarz, Markus J
本文就精神分裂症和抑郁症不同免疫状态的可能原因及其影响作一综述。它讨论了这样一个事实，在精神分裂症中，2型免疫反应的过度激活可能占主导地位，而在严重抑郁症中，1型和促炎性免疫反应可能被过度激活。这些不同免疫状态的结果是色氨酸/犬尿氨酸代谢中不同酶的激活和抑制，这可能导致精神分裂症患者过度强调N-甲基-D-天冬氨酸(NMDA)受体拮抗作用，抑郁症患者过度强调NMDA受体激动性作用，导致精神分裂症患者谷氨酸能功能低下，抑郁症患者谷氨酸能功能亢进。此外，在重度抑郁症中，1型和促炎性免疫反应的激活导致5-羟色胺降解增加和5-羟色胺能缺陷。目前的抗精神病药物和抗抑郁药物主要作用于多巴胺能-谷氨酸能和去甲肾上腺素-5-羟色胺能神经传递，而抗炎和免疫调节治疗可能更基本地作用于病理生理机制。然而，对这一概念的局限性进行了批判性的讨论。
This review focuses on possible causes and the impact of different immune states in schizophrenia and major depression. It discusses the fact that, in schizophrenia, an over-activation of the type 2 immune response may dominate, while the type 1 and the pro-inflammatory immune responses are over-activated in major depression. The consequence of these diverse immune states is the activation and, respectively, inhibition of different enzymes in tryptophan/kynurenine metabolism, which may lead to an overemphasis of N-methyl-D-aspartate (NMDA) receptor antagonism in schizophrenia and of NMDA-receptor agonism in depression, resulting in glutamatergic hypofunction in schizophrenia and glutamatergic hyperfunction in major depression. In addition, the activation of the type 1 and the pro-inflammatory immune responses in major depression result in increased serotonin degradation and a serotonergic deficit. While antipsychotics and antidepressants today mainly act on the dopaminergic-glutamatergic and the noradrenergic-serotonergic neurotransmission, anti-inflammatory and immune-modulating therapies might act more basically at the pathophysiological mechanism. The limitations of this concept, however, are critically discussed.