Schizophrenia is a complex, chronic mental health disorder whose heterogeneous genetic and neurobiological background influences early brain development, and whose precise etiology is still poorly understood. Schizophrenia is not characterized by gross brain pathology, but involves subtle pathological changes in neuronal populations and glial cells. Among the latter, astrocytes critically contribute to the regulation of early neurodevelopmental processes, and any dysfunctions in their morphological and functional maturation may lead to aberrant neurodevelopmental processes involved in the pathogenesis of schizophrenia, such as mitochondrial biogenesis, synaptogenesis, and glutamatergic and dopaminergic transmission. Studies of the mechanisms regulating astrocyte maturation may therefore improve our understanding of the cellular and molecular mechanisms underlying the pathogenesis of schizophrenia.

Emerging evidence for astrocyte dysfunction in schizophrenia

Cali C.;
2022-01-01

Abstract

Schizophrenia is a complex, chronic mental health disorder whose heterogeneous genetic and neurobiological background influences early brain development, and whose precise etiology is still poorly understood. Schizophrenia is not characterized by gross brain pathology, but involves subtle pathological changes in neuronal populations and glial cells. Among the latter, astrocytes critically contribute to the regulation of early neurodevelopmental processes, and any dysfunctions in their morphological and functional maturation may lead to aberrant neurodevelopmental processes involved in the pathogenesis of schizophrenia, such as mitochondrial biogenesis, synaptogenesis, and glutamatergic and dopaminergic transmission. Studies of the mechanisms regulating astrocyte maturation may therefore improve our understanding of the cellular and molecular mechanisms underlying the pathogenesis of schizophrenia.
2022
70
9
1585
1604
astrocytes; dopamine; gliotransmitter; mitochondria; schizophrenia
de Oliveira Figueiredo E.C.; Cali C.; Petrelli F.; Bezzi P.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/1885373
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