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Updated: May 7, 2026
Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Microglia as critical mediators linking perinatal immune stress to mental health trajectories
Ravikiran M Raju1,2,3, Caroline J Smith4
1Division of Newborn Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Insights
Early life immune activation and stress impact microglia, the brain's immune cells. This review links these changes to neurodevelopmental disorders like autism and neuropsychiatric conditions such as depression and schizophrenia.
Area of Science:
- Neuroscience
- Immunology
- Developmental Biology
Background:
- Neurodevelopmental and neuropsychiatric disorders lack effective therapies, necessitating research into their origins.
- Perinatal immune activation and stress are identified risk factors for these conditions.
- Microglia, brain immune cells, are sensitive to early life events and implicated in these disorders.
Purpose of the Study:
- To review literature on microglia-specific alterations due to early life immune activation and/or stress.
- To examine microglial interactions with neural synapses and circuits in this context.
- To connect these microglial changes to the pathogenesis of autism, depression, and schizophrenia.
Main Methods:
- Literature review focusing on studies of microglia, early life insults, and neurodevelopmental/neuropsychiatric disorders.
- Emphasis on research linking microglial function to synaptic and circuit alterations.
- Synthesis of findings related to autism, depression, and schizophrenia.
Main Results:
- Early life immune activation and stress induce specific changes in microglia.
- These microglial alterations affect neural synapses and circuits.
- Evidence suggests a role for these microglial changes in the development of autism, depression, and schizophrenia.
Conclusions:
- Microglia are a critical link between early life insults and the development of neurodevelopmental and neuropsychiatric disorders.
- Understanding microglia-specific mechanisms is key to bridging the gap between developmental insults and disease.
- Further mechanistic research is needed to explore therapeutic targets.
Abstract:
Neurodevelopmental and neuropsychiatric disorders that emerge in childhood (such as autism) and adolescence (such as depression and schizophrenia) currently lack broadly effective therapies, underlying an urgent need to better understand their etiology. While each disorder has its own set of complex genetic and environmental risk factors, perinatal exposure to intense immune activation and/or stress has been linked to increased disease risk. Microglia, the resident immune cells of the brain, are impacted in each disorder and exquisitely sensitive to early life experience. Here, we review the literature suggesting microglia-specific changes in response to early life immune activation and/or stress with an emphasis on microglial interactions with neural synapses and circuits. We also review the existing literature linking these findings to microglia-specific changes in the brain in autism, depression, and schizophrenia. Our goal is to bridge the gap between developmental insults and the subsequent pathogenesis of these disorders, highlighting key areas for future mechanistic work.
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