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This page is an AI-assisted Turkish summary of the study presented at the 26th World Congress of Psychiatry. The study belongs to the presenting authors; please refer to the original source when citing it.

Association of the complement C3–hippocampus pathway with mood symptoms in offspring of parents with bipolar disorder

The role of the complement c3-hippocampus pathway in relation with mood symptoms in offspring of parents with bipolar disorder

Offspring of parents with bipolar disorder who have subthreshold symptoms show reduced peripheral complement C3 levels and left hippocampus–left cerebellum connectivity, and this connectivity partially mediates the relationship between C3 and depressive symptoms.

The study aimed to examine the relationship between complement component 3 (C3) levels, hippocampal function, and mood symptoms in offspring of parents with bipolar disorder (BD) who are at familial risk for mood disorders. Unaffected offspring of parents with BD, with subthreshold symptoms (symptomatic offspring, SO, N=31) and without subthreshold symptoms (asymptomatic offspring, AO, N=39), and matched healthy controls (HC, N=41) were recruited; peripheral C3 levels were measured, hippocampal functional connectivity (FC) was assessed using resting-state functional magnetic resonance imaging, and the direction of connectivity was verified using spectral dynamic causal modeling (spDCM). Compared with both the AO and HC groups, the SO group had significantly lower peripheral C3 levels (F2,108=23.651; p<0.001) and reduced left hippocampus–left cerebellum FC (F2,108=8.541; p<0.001). Left hippocampus–left cerebellum FC partially mediated the relationship between C3 levels and depressive symptoms in the SO group (bootstrap 95% CI=-4.1168 to -0.1569), whereas no mediation was detected in the AO (95% CI=-0.3479 to 0.1317) or HC (95% CI=-0.3297 to 0.0885) groups; this connection was bidirectional in all three groups. The findings suggest that a C3–hippocampus–depressive symptom pathway may underlie the heightened vulnerability of individuals with both familial and symptomatic risk. According to the authors, this offers novel neuroinflammatory markers and targets for early identification and intervention in high-risk individuals.

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