Over Complement

Causing cognitive deficiencies and psychosis, schizophrenia is a serious mental disorder known to be highly heritable, yet its underlying causes are difficult to grasp. Among many genetic factors linked to this condition, the strongest association is with a gene involved in the immune system, known as complement C4. Scientists are closing in on how it contributes to schizophrenia, with recent evidence suggesting it triggers excessive pruning of connections between neurons (synapses) at adolescence, and now new work looking at the impact of excess C4 during development. Within the brain’s prefrontal cortex of mice (pictured, with cell nuclei in blue), extra C4 in pyramidal neurons (in green) encourages microglia (in magenta) to engulf and destroy more synapses, reducing neuronal connectivity, and leads to neurological defects and reduced social behaviours reminiscent of schizophrenia. Thinking about treatment, intervening while neural circuits are sensitive to the effects of C4 could represent an opportunity to reduce disease progression.

Written by Emmanuelle Briolat

Emmanuelle Briolat

Writer

A researcher specialising in visual signals in Lepidoptera, camouflage and the effects of light pollution, Emmanuelle’s writing covers a range of topics, from biomedical research to children’s books about moth defences.

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• IMAGE BY THANH P. H. NGUYEN, CRUZ-MARTIN LAB, BOSTON UNIVERSITY
• Department of Biology, Boston University, Boston, MA, USA
• Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)
• Published in PLOS Biology, January 2020