背景:精神病学迫切需要可靠的生物标志物。新型神经黑色素敏感磁共振成像(NM-MRI)序列提供了一种时间高效且非侵入性的方法来研究体内人脑。这可以深入了解多巴胺能信号的代谢物,并可能为精神分裂症(SCZ)患者的潜在多巴胺能改变提供进一步的证据。本系统综述提供了SCZ与SCZ中使用神经黑色素敏感序列的病例对照研究的荟萃分析。健康对照(HC)。方法:根据预定义的搜索词和纳入标准,在PubMed上提取研究。采用逆方差法的固定和随机效应模型进行荟萃分析,计算了τ2的DerSimonian-Laird估计和Cohen'sd。使用漏斗图评估偏差。主要研究结果是HC和SCZ之间黑质的对比噪声比(CNR)。结果:k=6项研究的总样本包括n=183例和n=162例对照。在所有研究中,我们发现黑质中的CNR显着升高(d=0.42[0.187;0.655],与对照组相比,z=3.521,p<0.001)。我们发现蓝斑对照区没有显着差异(d=-0.07[-0.446;0.302],z=-0.192,p=0.847),后者的CNR仅在k=3项研究中报道。结论:与对照组相比,病例黑质中的CNR显着升高。我们的结果支持神经黑色素作为精神分裂症多巴胺能功能障碍的候选生物标志物。进一步的研究需要评估这个候选标记,纵向队列和解决疾病状态的潜在影响,药物和与症状的相关性。
Background: Psychiatry is in urgent need of reliable biomarkers. Novel
neuromelanin-sensitive magnetic resonance imaging (NM-MRI) sequences provide a time-efficient and non-invasive way to investigate the human brain in-vivo. This gives insight into the metabolites of dopaminergic signaling and may provide further evidence for potential dopaminergic alterations in patients with schizophrenia (SCZ). The present systematic review provides a meta-analysis of
case-control studies using
neuromelanin-sensitive sequences in SCZ vs. healthy controls (HC). Methods: According to predefined search terms and inclusion criteria studies were extracted on PubMed. Meta-analyses with a fixed and random-effects model with inverse variance method, DerSimonian-Laird estimator for τ2, and Cohen\'s d were calculated. Bias was assessed using funnel plots. The primary study outcome was contrast-to-noise ratio (CNR) in the substantia nigra compared between HC and SCZ. Results: The total sample of k = 6 studies included n = 183 cases and n = 162 controls. Across all studies we found a significant elevation of CNR in the substantia nigra (d = 0.42 [0.187; 0.655], z = 3.521, p < 0.001) in cases compared to controls. We found no significant difference in the control region of locus coeruleus (d = -0.07 [-0.446; 0.302], z = -0.192, p = 0.847), with CNR for the latter only reported in k = 3 studies. Conclusion: CNR in the substantia nigra were significantly elevated in cases compared to controls. Our results support
neuromelanin as a candidate biomarker for dopaminergic dysfunction in schizophrenia. Further studies need to assess this candidate marker in large, longitudinal cohorts and address potential effects of disease state, medication and correlations with symptoms.