While attention is widely recognised as central to perception, the term is often used to mean very different things. Prominent theories of attention — notably the premotor theory — relate it to planned or executed eye movements. This contrasts with the notion of attention as a gain control process that weights the information carried by different sensory channels. We draw upon recent advances in theoretical neurobiology to argue for a distinction between attentional gain mechanisms and salience attribution. The former depends (...) upon estimating the precision of sensory data, while the latter is a consequence of the need to actively engage with the sensorium. Having established this distinction, we consider the intimate relationship between attention and salience. (shrink)

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: why 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: translation, unification, and simulation. 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? (shrink)

This commentary focuses upon the relationship between two themes in the target article: the ways in which a Markov blanket may be defined and the role of precision and salience in mediating the interactions between what is internal and external to a system. These each rest upon the different perspectives we might take while “choosing” a Markov blanket.

This article proposes a formal model that integrates cognitive and psychodynamic psychotherapeutic models of psychopathy to show how two major psychopathic traits called lacks remorse and self-aggrandizing can be understood as a form of abnormal Bayesian inference about the self. This model draws on the predictive coding (i.e., active inference) framework, a neurobiologically plausible explanatory framework for message passing in the brain that is formalized in terms of hierarchical Bayesian inference. In summary, this model proposes that these two cardinal psychopathic (...) traits reflect entrenched maladaptive Bayesian inferences about the self, which defend against the experience of deep-seated, self-related negative emotions, specifically shame and worthlessness. Support for the model in extant research on the neurobiology of psychopathy and quantitative simulations are provided. Finally, we offer a preliminary overview of a novel treatment for psychopathy that rests on our Bayesian formulation. (shrink)

This commentary suggests that, although Markov blankets may have different interpretations in different systems, these distinctions rest not upon the type of blanket, but upon the model that determines the blanket. As an example, the conditions for a model in which the Markov blanket may be interpretable as a physical (spatial) boundary are considered.