Connecting Neurobiological Features with Interregional Dysconnectivity in Social-Cognitive Impairments of Schizophrenia

Schizophrenia (SZ) is a devastating psychiatric disorder affecting about 1% of the world's population. Social-cognitive impairments in SZ prevent positive social interactions and lead to progressive social withdrawal. The neurobiological underpinnings of social-cognitive symptoms remain poorly...

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Bibliographic Details
Published in:International journal of molecular sciences 2023-04, Vol.24 (9), p.7680
Main Authors: Adraoui, Florian W, Douw, Linda, Martens, Gerard J M, Maas, Dorien A
Format: Article
Language:English
Subjects:
Aspartate
Brain - pathology
Brain research
Cognition & reasoning
Cognitive Dysfunction
Drug development
EEG
Electroencephalography
Glutamate receptors
Humans
Inflammation
Magnetic Resonance Imaging
Mental disorders
Methyl aspartate
Myelination
N-Methyl-D-aspartic acid receptors
Neural networks
Neurobiology
Oxidative stress
Review
Schizophrenia
Social aspects
Social factors
Social interaction
Social interactions
Social networks
Social organization
Therapeutic targets
Withdrawal
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Summary:Schizophrenia (SZ) is a devastating psychiatric disorder affecting about 1% of the world's population. Social-cognitive impairments in SZ prevent positive social interactions and lead to progressive social withdrawal. The neurobiological underpinnings of social-cognitive symptoms remain poorly understood, which hinders the development of novel treatments. At the whole-brain level, an abnormal activation of social brain regions and interregional dysconnectivity within social-cognitive brain networks have been identified as major contributors to these symptoms. At the cellular and subcellular levels, an interplay between oxidative stress, neuroinflammation and N-methyl-D-aspartate receptor hypofunction is thought to underly SZ pathology. However, it is not clear how these molecular processes are linked with interregional dysconnectivity in the genesis of social-cognitive symptoms. Here, we aim to bridge the gap between macroscale (connectivity analyses) and microscale (molecular and cellular mechanistic) knowledge by proposing impaired myelination and the disinhibition of local microcircuits as possible causative biological pathways leading to dysconnectivity and abnormal activity of the social brain. Furthermore, we recommend electroencephalography as a promising translational technique that can foster pre-clinical drug development and discuss attractive drug targets for the treatment of social-cognitive symptoms in SZ.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms24097680