Schizophrenia is a severe and clinically heterogenous mental disorder affecting approximately 1% of the population worldwide. Despite tremendous achievements in the field of schizophrenia research, its precise aetiology remains elusive. Besides dysfunctional neuronal signalling, the pathophysiology of schizophrenia appears to involve molecular and functional abnormalities in glial cells, including astrocytes. This article provides a concise overview of the current evidence supporting altered astrocyte activity in schizophrenia, which ranges from findings obtained from post-mortem immunohistochemical analyses, genetic association studies and transcriptomic investigations, as well as from experimental investigations of astrocyte functions in animal models. Integrating the existing data from these research areas strongly suggests that astrocytes have the capacity to critically affect key neurodevelopmental and homeostatic processes pertaining to schizophrenia pathogenesis, including glutamatergic signalling, synaptogenesis, synaptic pruning and myelination. The further elucidation of astrocytes functions in health and disease may, therefore, offer new insights into how these glial cells contribute to abnormal brain development and functioning underlying this debilitating mental disorder.
Keyphrases
- bipolar disorder
- induced apoptosis
- mental health
- public health
- cell cycle arrest
- healthcare
- dna methylation
- early onset
- genome wide
- machine learning
- big data
- gene expression
- multiple sclerosis
- artificial intelligence
- climate change
- single cell
- rna seq
- cell death
- signaling pathway
- spinal cord
- brain injury
- cerebral ischemia
- deep learning
- copy number
- cell proliferation
- blood brain barrier