Can electroconvulsive therapy attenuate glial stress in schizophrenia? Longitudinal evidence from serum GFAP and S100B.

BACKGROUND

Glial dysfunction has been implicated in schizophrenia, yet ECT's effects on glial biomarkers remain poorly understood. This study investigated longitudinal changes in serum GFAP and S100B in patients with schizophrenia treated with antipsychotic medication alone or combined with ECT.

METHODS

Seventy-six patients with schizophrenia (37 ECT + medication; 39 medication alone) and 36 healthy controls were enrolled. Serum GFAP and S100B were measured at baseline, 24 h post-first ECT session, and at three-month follow-up. Symptom severity was assessed using PANSS. Longitudinal changes were analyzed using repeated measures ANOVA and paired t-tests.

RESULTS

Both patient groups showed elevated baseline S100B compared with controls. In the ECT group, S100B increased acutely after the first session (p = 0.002) then normalized at three months. In the medication-only group, S100B significantly increased over follow-up (p = 0.047). Baseline GFAP was elevated in the ECT group with a decreasing trend at three months (p = 0.086), while remaining stable in the medication-only group. No significant correlations emerged between biomarker changes and PANSS improvement.

CONCLUSIONS

Antipsychotic monotherapy may be insufficient to modify ongoing glial stress, whereas ECT is associated with transient glial activation followed by longer-term normalization. These distinct S100B trajectories suggest that ECT's therapeutic effects may involve dynamic modulation of glial function, providing preliminary evidence for glia-related mechanisms underlying ECT in schizophrenia.