Dissecting the neurobiology of linguistic disorganisation and impoverishment in schizophrenia

Schizophrenia provides a quintessential disease model of how disturbances in the molecular mechanisms of neurodevelopment lead to disruptions in the emergence of cognition. The central and often persistent feature of this illness is the disorganisation and impoverishment of language and related expr...

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Published in:Seminars in cell & developmental biology 2022-09, Vol.129, p.47-60
Main Author: Palaniyappan, Lena
Format: Article
Language:English
Subjects:
Disorganisation
Excitotoxicity
Formal thought disorder
FOXP2
GABA
Inhibition
Language
Oscillations
Schizophrenia
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Summary:Schizophrenia provides a quintessential disease model of how disturbances in the molecular mechanisms of neurodevelopment lead to disruptions in the emergence of cognition. The central and often persistent feature of this illness is the disorganisation and impoverishment of language and related expressive behaviours. Though clinically more prominent, the periodic perceptual distortions characterised as psychosis are non-specific and often episodic. While several insights into psychosis have been gained based on study of the dopaminergic system, the mechanistic basis of linguistic disorganisation and impoverishment is still elusive. Key findings from cellular to systems-level studies highlight the role of ubiquitous, inhibitory processes in language production. Dysregulation of these processes at critical time periods, in key brain areas, provides a surprisingly parsimonious account of linguistic disorganisation and impoverishment in schizophrenia. This review links the notion of excitatory/inhibitory (E/I) imbalance at cortical microcircuits to the expression of language behaviour characteristic of schizophrenia, through the building blocks of neurochemistry, neurophysiology, and neurocognition. •Disorganized and impoverished language and related expressive behaviours (LDI) are core features of schizophrenia.•Disinhibitory motifs both at the microcircuit (glutamate/GABA-based) and distributed network level are critical for language.•LDI can be traced from cellular to systems-level as a dysregulation of inhibition or bias processing.•Susceptibility to E/I imbalance affects oscillatory and specific network-level dyconnectivity producing LDI in schizophrenia.
ISSN:1084-9521
1096-3634
DOI:10.1016/j.semcdb.2021.08.015