4.7 Review

How Can Animal Models Inform the Understanding of Cognitive Inflexibility in Patients with Anorexia Nervosa?

Journal

JOURNAL OF CLINICAL MEDICINE
Volume 11, Issue 9, Pages -

Publisher

MDPI
DOI: 10.3390/jcm11092594

Keywords

anorexia nervosa; activity-based anorexia; cognitive flexibility; animal models; prefrontal cortex; serotonin; dopamine

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Deficits in cognitive flexibility are commonly observed in patients with anorexia nervosa (AN). These deficits are believed to contribute to the persistence of the disorder, as they result in deeply ingrained patterns of thought and behavior that are resistant to change. Neurobiological factors that drive cognitive inflexibility share similarities with the abnormal brain function observed in AN patients, such as disrupted prefrontal cortical function and dysregulated dopamine and serotonin neurotransmitter systems. The activity-based anorexia (ABA) model replicates key features of AN in human patients, making it a valuable tool for investigating the cognitive and neurobiological causes of pathological weight loss. This review aims to explore the relationship between AN, neural function, and cognitive flexibility in human patients, and highlight how behavioral neuroscience techniques can enhance the use of animal models to advance the development of novel therapies.
Deficits in cognitive flexibility are consistently seen in patients with anorexia nervosa (AN). This type of cognitive impairment is thought to be associated with the persistence of AN because it leads to deeply ingrained patterns of thought and behaviour that are highly resistant to change. Neurobiological drivers of cognitive inflexibility have some commonalities with the abnormal brain functional outcomes described in patients with AN, including disrupted prefrontal cortical function, and dysregulated dopamine and serotonin neurotransmitter systems. The activity-based anorexia (ABA) model recapitulates the key features of AN in human patients, including rapid weight loss caused by self-starvation and hyperactivity, supporting its application in investigating the cognitive and neurobiological causes of pathological weight loss. The aim of this review is to describe the relationship between AN, neural function and cognitive flexibility in human patients, and to highlight how new techniques in behavioural neuroscience can improve the utility of animal models of AN to inform the development of novel therapeutics.

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