About this Research Topic
Despite distinct diagnostic criteria, schizophrenia (SZ), bipolar disorder (BD), and major depressive disorder (MDD), show significant overlap in symptoms and manifestations. Neurocognitive deficits, such as impairments in executive functioning, attention, and memory are especially prevalent in SZ, but can also observed in both BD and MDD, with type I BD showing higher frequencies of these impairments. In addition, impairments in social cognition (i.e. deficits in the recognition and perception of socio-emotional cues, social inference, and the theory of mind) can also be recorded across these disorders but with different grades of severity and frequency. SZ often involves severe and pervasive social cognitive deficits. BD patients can experience moderate impairments both in euthymic and symptomatic states, while social cognition in patients with MDD is more variable, generally presenting milder impairments influenced by the severity of depressive symptoms.
While some similarities exist in BD and MDD cognitive profiles, and occasional overlaps with SZ, the distinct and shared mechanisms driving cognitive impairments across these disorders remain unclear.
First, cognitive dysfunction has been observed in BD and SZ before clinical manifestations and in first-degree relatives, especially in subjects with SZ and patients with BD with psychotic features, suggesting that genetic factors play a role in these deficits and might signal the upcoming onset of the illness. Similarly, in MDD, the risk factor is also tied to the patient’s genetic profile and influenced by environmental factors.
Second, neuroimaging findings have often found contrasting results in terms of cerebral alterations associated to cognition. In SZ, cognitive dysfunction appears to be linked to disruptions in brain activity and connectivity pathways, with results indicating both increased and decreased connectivity. Moreover, deficits in social cognition have been found to be related to hypoactivation in the right inferior occipital gyrus, amygdala, hippocampus and anterior cingulate cortex. In BD, disruptions are noted in brain networks like the default mode network (DMN) and cognitive control network (CEN). MDD research also indicates functional synchrony disruptions, with disturbances in connectivity within and between brain networks, including the DMN, frontoparietal (FPN), and salience (SN) networks.
Finally, alterations in immune-inflammatory responses may further contribute to these shared cognitive impairments in SZ, BD, and MDD, impacting cognitive functioning. Research has yielded mixed findings on the nature and extent of these deficits across disorders, with few studies employing a comprehensive, transdiagnostic approach to characterize them.
Understanding the physiological and biological mechanisms underlying cognitive impairment in SZ, BD, and MDD remains challenging. Therefore, this Research Topic aims to clarify the prevalence and characteristics of cognitive impairments across these disorders and explore factors associated with their onset providing insights into shared and unique mechanisms in SZ, BD, and MDD.
Submissions addressing neurobiological findings, and neuroimaging studies relating to cognitive deficits in these disorders are welcome, with a strong emphasis on transdiagnostic studies involving SZ, BD, and MDD populations.
To provide a transdisciplinary and comprehensive overview of the topic, foster collaboration across disciplines, we welcome submissions focusing on, but not limited to, the following:
- Factors contributing to cognitive deficits in SZ, BD, and MDD.
- Neurobiological, neuroimaging, and electrophysiological correlates of cognitive impairment in SZ, BD, and MDD.
- Investigations into genetic and environmental risk factors linked to cognitive deficits in these disorders.
- Temporal dynamics of cognitive deficits: longitudinal studies on cognitive deficits across different stages of illness.
- Reports of changes in cognitive functioning following pharmacological intervention.
- Application and efficacy of cognitive interventions in patients with SZ, BD, or MDD.
- Application of AI in the use of multimodal data for the detection of cognitive deficits.
While some similarities exist in BD and MDD cognitive profiles, and occasional overlaps with SZ, the distinct and shared mechanisms driving cognitive impairments across these disorders remain unclear.
First, cognitive dysfunction has been observed in BD and SZ before clinical manifestations and in first-degree relatives, especially in subjects with SZ and patients with BD with psychotic features, suggesting that genetic factors play a role in these deficits and might signal the upcoming onset of the illness. Similarly, in MDD, the risk factor is also tied to the patient’s genetic profile and influenced by environmental factors.
Second, neuroimaging findings have often found contrasting results in terms of cerebral alterations associated to cognition. In SZ, cognitive dysfunction appears to be linked to disruptions in brain activity and connectivity pathways, with results indicating both increased and decreased connectivity. Moreover, deficits in social cognition have been found to be related to hypoactivation in the right inferior occipital gyrus, amygdala, hippocampus and anterior cingulate cortex. In BD, disruptions are noted in brain networks like the default mode network (DMN) and cognitive control network (CEN). MDD research also indicates functional synchrony disruptions, with disturbances in connectivity within and between brain networks, including the DMN, frontoparietal (FPN), and salience (SN) networks.
Finally, alterations in immune-inflammatory responses may further contribute to these shared cognitive impairments in SZ, BD, and MDD, impacting cognitive functioning. Research has yielded mixed findings on the nature and extent of these deficits across disorders, with few studies employing a comprehensive, transdiagnostic approach to characterize them.
Understanding the physiological and biological mechanisms underlying cognitive impairment in SZ, BD, and MDD remains challenging. Therefore, this Research Topic aims to clarify the prevalence and characteristics of cognitive impairments across these disorders and explore factors associated with their onset providing insights into shared and unique mechanisms in SZ, BD, and MDD.
Submissions addressing neurobiological findings, and neuroimaging studies relating to cognitive deficits in these disorders are welcome, with a strong emphasis on transdiagnostic studies involving SZ, BD, and MDD populations.
To provide a transdisciplinary and comprehensive overview of the topic, foster collaboration across disciplines, we welcome submissions focusing on, but not limited to, the following:
- Factors contributing to cognitive deficits in SZ, BD, and MDD.
- Neurobiological, neuroimaging, and electrophysiological correlates of cognitive impairment in SZ, BD, and MDD.
- Investigations into genetic and environmental risk factors linked to cognitive deficits in these disorders.
- Temporal dynamics of cognitive deficits: longitudinal studies on cognitive deficits across different stages of illness.
- Reports of changes in cognitive functioning following pharmacological intervention.
- Application and efficacy of cognitive interventions in patients with SZ, BD, or MDD.
- Application of AI in the use of multimodal data for the detection of cognitive deficits.
Keywords: cognitive deficits, schizophrenia, bipolar disorder, neurocognition, social cognition, neuroimaging, major depressive disorder
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
