Bhat Anjali, Parr Thomas, Ramstead Maxwell, Friston Karl
Wellcome Centre for Human Neuroimaging, London, UK.
Division of Psychiatry, University College London, London, UK.
Biol Philos. 2021;36(3):27. doi: 10.1007/s10539-021-09801-6. Epub 2021 Apr 30.
There is a steadily growing literature on the role of the immune system in psychiatric disorders. So far, these advances have largely taken the form of correlations between specific aspects of inflammation (e.g. blood plasma levels of inflammatory markers, genetic mutations in immune pathways, viral or bacterial infection) with the development of neuropsychiatric conditions such as autism, bipolar disorder, schizophrenia and depression. A fundamental question remains open: are psychiatric disorders and immune responses intertwined? To address this would require a step back from a historical mind-body dualism that has created such a dichotomy. We propose three contributions of active inference when addressing this question: , , and To illustrate these contributions, we consider the following questions. Is there an immunological analogue of sensory attenuation? Is there a common generative model that the brain and immune system jointly optimise? Can the immune response and psychiatric illness both be explained in terms of self-organising systems responding to threatening stimuli in their external environment, whether those stimuli happen to be pathogens, predators, or people? Does false inference at an immunological level alter the message passing at a psychological level (or vice versa) through a principled exchange between the two systems?
关于免疫系统在精神疾病中作用的文献正在稳步增加。到目前为止,这些进展主要表现为炎症的特定方面(例如炎症标志物的血浆水平、免疫途径中的基因突变、病毒或细菌感染)与神经精神疾病(如自闭症、双相情感障碍、精神分裂症和抑郁症)的发展之间的相关性。一个基本问题仍然悬而未决:精神疾病与免疫反应是否相互交织?要解决这个问题,需要从造成这种二分法的历史身心二元论中退一步。我们提出在解决这个问题时主动推理的三个贡献: , ,以及 为了说明这些贡献,我们考虑以下问题。是否存在感觉衰减的免疫学类似物?大脑和免疫系统是否共同优化一个共同的生成模型?免疫反应和精神疾病是否都可以用自组织系统对其外部环境中的威胁性刺激做出反应来解释,无论这些刺激碰巧是病原体、捕食者还是人?免疫水平上的错误推理是否会通过两个系统之间有原则的交换改变心理水平上的信息传递(反之亦然)?