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
MicroRNAs, as key regulators in gene expression, may hold the key to understanding Alzheimer disease (AD) pathogenesis and diagnosis. To explore the expression level of miR-106b-3p in the serum of AD Show more
MicroRNAs, as key regulators in gene expression, may hold the key to understanding Alzheimer disease (AD) pathogenesis and diagnosis. To explore the expression level of miR-106b-3p in the serum of AD patients, and evaluate its diagnostic value for AD. A total of 250 AD patients and 200 healthy controls were enrolled. Real-time quantitative PCR with fluorescence detection was used to determine the relative expression level of miR-106b-3p. Correlation was analyzed by the Pearson linear correlation analysis. The receiver operating characteristic was used to evaluate the diagnostic efficacy of serum miR-106b-3p for AD. In vitro AD cellular models were established to explore the potential mechanism of miR-106b-3p in AD. The expression of miR-106b-3p in the serum of AD patients is significantly elevated, and its level is negatively correlated with the MMSE score. ROC curve analysis shows that it has certain diagnostic value. miR-106b-3p is a risk factor associated with AD. In addition, miR-106b-3p targets BDNF, affects the functions of SH-SY5Y cells, and promotes the occurrence and development of AD. Serum miR-106b-3p is significantly elevated in AD and may serve as a diagnostic biomarker. Preliminary evidence suggests it promotes AD progression by targeting BDNF, highlighting its potential as a therapeutic target for early intervention. Show less