治疗耐药精神分裂症的分子基础:与治疗响应性精神分裂症的假定不同的神经生物学
Annarita Barone1, Licia Vellucci1,2, Mariateresa Ciccarelli1
1Section of Psychiatry, Laboratory of Translational and Molecular Psychiatry, Unit of Treatment-Resistant Psychosis, Department of Neuroscience, Reproductive Sciences and Dentistry, University Medical School of Naples "Federico II", Via Pansini 5, 80131 Naples, Italy.
耐治疗精神分裂症 (TRS) 涉及多巴胺以外的复杂生物机制. 了解这些免疫,代谢和突触因素是开发有针对性的治疗方法和生物标志物以改善患者护理的关键.
科学领域:
- 神经科学是一个神经科学.
- 精神病学是一个精神病学.
- 分子生物学分子生物学
背景情况:
- 耐治疗精神分裂症 (TRS) 影响了相当一部分精神分裂症患者,带来了独特的挑战.
- TRS病理生理学超越了多巴胺功能障碍,表明其他生物途径的参与.
研究的目的:
- 审查目前对TRS.分子和细胞基础的理解.
- 探索TRS的潜在生物标志物和新型治疗点.
主要方法:
- 关于分子,细胞,遗传,蛋白质组,代谢组和神经成像研究的综合文献综述.
- 从临床前模型和死后大脑研究中分析数据.
主要成果:
- TRS与谷氨酸信号,刺激/抑制平衡,D-氨基酸代谢,神经炎症,氧化应激和器官功能障碍的改变有关.
- 基因组,蛋白质组和代谢组数据表明TRS有着独特的神经生物学基础.
- 神经成像揭示了与治疗响应患者相比,TRS患者的大脑的结构和连接差异.
结论:
- 目前的发现支持从多巴胺假设转向TRS的多因素模型,包括免疫,代谢和突触元素.
- 确定这些因素的相互作用可能会导致预测抗精神病反应的生物标志物.
- 更深入的生物学洞察力和早期识别对于TRS个性化治疗策略至关重要.
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