Neuroplasticity dysregulation is implicated in the early pathophysiology of schizophrenia. Nogo-A, a myelin- and neuron-associated inhibitor of structural plasticity, has been less studied in first-ep Show more
Neuroplasticity dysregulation is implicated in the early pathophysiology of schizophrenia. Nogo-A, a myelin- and neuron-associated inhibitor of structural plasticity, has been less studied in first-episode schizophrenia (FES) than brain-derived neurotrophic factor (BDNF). This study examined short-term changes in serum Nogo-A and BDNF in drug-naïve patients with FES. Thirty-nine drug-naïve FES patients and 43 healthy controls (HC) were assessed. Serum Nogo-A and BDNF were measured at baseline in both groups and re-measured in FES after achieving ≥20 % reduction in Positive and Negative Syndrome Scale total score (PANSS). Baseline Nogo-A levels were higher in FES than HC (p = .022) and increased further after treatment (p < .001). Baseline BDNF did not differ between groups (p = .069) and showed no significant change after treatment (p = .094). PANSS total and subscale scores decreased significantly after treatment (all p < .001). Baseline Nogo-A modestly discriminated FES from HC (AUC = 0.648, 95 % CI = 0.53-0.77, sensitivity 66.7 %, specificity 60.5 %). In multivariable analysis, only smoking independently predicted FES (OR = 3.69, 95 % CI = 1.48-9.23, p = .005), whereas Nogo-A was not retained. Serum Nogo-A is elevated at illness onset in FES and increases during early treatment, suggesting that peripheral Nogo-A may be associated with early illness-related and/or treatment-related biological changes. Although Nogo-A does not show sufficient performance as a stand-alone diagnostic biomarker, these findings should be interpreted cautiously given the relatively small sample size and naturalistic treatment design. Nogo-A may warrant further investigation as part of broader multi-marker approaches in early schizophrenia. Show less