Scholarlink

<p>The tryptophan (TRP)-kynurenine (KYN) pathway is involved in the pathogenesis of schizophrenia. This study aimed to investigate the levels of TRP-KYN metabolites in serum and urine of patients with first-episode schizophrenia (FES) and their association with clinical manifestations. This study included 38 drug-naive patients with FES and 43 healthy controls (HCs). Clinical symptoms were evaluated using the Positive and Negative Syndrome Scale (PANSS). Levels of TRP-KYN metabolites in serum and urine were quantified. Patients with FES showed significantly higher serum quinolinic acid/kynurenic acid (QUIN/KYNA) ratio and urine KYN/TRP ratio compared to HCs, while neuroprotective metabolites, including serum KYNA, xanthurenic acid (XA), and urine picolinic acid (PIC) levels, were significantly reduced, along with a decreased urine PIC/QUIN ratio (<i>p</i> &lt; 0.05). The urine KYNA/KYN ratio was negatively correlated with PANSS general psychopathology scores (<i>r</i> = -0.35, <i>p</i> = 0.04) and with PANSS total scores (<i>r</i> = -0.35, <i>p</i> = 0.046). Patients with FES exhibited dysregulation of the peripheral TRP-KYN pathway, characterized by an increased neurotoxic-to-neuroprotective QUIN/KYNA ratio and reduced levels of neuroprotective metabolites. This shift towards increased neurotoxic product generation suggests that the dysregulation of the TRP-KYN pathway could play a role in the pathophysiology of schizophrenia.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Peripheral tryptophan-kynurenine pathway dysfunction in first-episode schizophrenia

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年1月18日

查看全文
  • Mian Li,
  • Yue Wu,
  • Yan Xu,
  • Xin Huang,
  • Kerun Gao,
  • Nannan Hu,
  • Shuangyue Zhu,
  • Chengpeng Wang,
  • Sugai Liang

摘要

The tryptophan (TRP)-kynurenine (KYN) pathway is involved in the pathogenesis of schizophrenia. This study aimed to investigate the levels of TRP-KYN metabolites in serum and urine of patients with first-episode schizophrenia (FES) and their association with clinical manifestations. This study included 38 drug-naive patients with FES and 43 healthy controls (HCs). Clinical symptoms were evaluated using the Positive and Negative Syndrome Scale (PANSS). Levels of TRP-KYN metabolites in serum and urine were quantified. Patients with FES showed significantly higher serum quinolinic acid/kynurenic acid (QUIN/KYNA) ratio and urine KYN/TRP ratio compared to HCs, while neuroprotective metabolites, including serum KYNA, xanthurenic acid (XA), and urine picolinic acid (PIC) levels, were significantly reduced, along with a decreased urine PIC/QUIN ratio (p < 0.05). The urine KYNA/KYN ratio was negatively correlated with PANSS general psychopathology scores (r = -0.35, p = 0.04) and with PANSS total scores (r = -0.35, p = 0.046). Patients with FES exhibited dysregulation of the peripheral TRP-KYN pathway, characterized by an increased neurotoxic-to-neuroprotective QUIN/KYNA ratio and reduced levels of neuroprotective metabolites. This shift towards increased neurotoxic product generation suggests that the dysregulation of the TRP-KYN pathway could play a role in the pathophysiology of schizophrenia.