期刊
NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
卷 129, 期 -, 页码 389-421出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neubiorev.2021.07.015
关键词
Maternal immune activation; Neurodevelopment; Rodent; Brain; Gene expression; Transcriptomic; Epigenetic; Systematic review
资金
- BBSRC DTP studentships
By systematically reviewing 118 studies, it was found that maternal immune activation (mIA) during pregnancy can cause changes in the transcriptome and epigenome of specific offspring brain regions, including elevated inflammatory markers and reduced myelin and GABA signaling proteins. Disturbed epigenetic markers at nine genes supported mIA-driven epigenetic modulation of transcription.
Maternal immune activation (mIA) during pregnancy is hypothesised to disrupt offspring neurodevelopment and predispose offspring to neurodevelopmental disorders such as schizophrenia. Rodent models of mIA have explored possible mechanisms underlying this paradigm and provide a vital tool for preclinical research. However, a comprehensive analysis of the molecular changes that occur in mIA-models is lacking, hindering identification of robust clinical targets. This systematic review assesses mIA-driven transcriptomic and epigenomic alterations in specific offspring brain regions. Across 118 studies, we focus on 88 candidate genes and show replicated changes in expression in critical functional areas, including elevated inflammatory markers, and reduced myelin and GABAergic signalling proteins. Further, disturbed epigenetic markers at nine of these genes support mIA-driven epigenetic modulation of transcription. Overall, our results demonstrate that current outcome measures have direct relevance for the hypothesised pathology of schizophrenia and emphasise the importance of mIA-models in contributing to the understanding of biological pathways impacted by mIA and the discovery of new drug targets.
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