在精神分裂症中尾状核的头部微质-神经元相互作用的超结构性障碍
Natalya A Uranova1, Olga V Vikhreva2, Valentina I Rakhmanova2
1Laboratory of Clinical Neuropathology, Mental Health Research Center, Kashirskoe Shosse 34, 115522, Moscow, Russia. uranovan@mail.ru.
European archives of psychiatry and clinical neuroscience
|December 29, 2024
概括
精神分裂症改变了卫星微质细胞 (SatMg) 和尾状核中的神经元之间的相互作用. 这些变化涉及线粒体功能障碍和微质内内的压力,可能导致精神分裂症患者的神经元衰老.
科学领域:
- 神经科学是一个神经科学.
- 细胞生物学 细胞生物学
- 精神病学是一个精神病学.
背景情况:
- 之前的研究发现了精神分裂症前额叶皮质中微质神经元相互作用的改变.
- 卫星微质细胞 (SatMg) 是一种特定类型的微质细胞,与神经元密切相关.
研究的目的:
- 研究精神分裂症尾状核中微质神经元相互作用的潜在失调.
- 检查精神分裂症患者尾状核中卫星微质细胞和相邻神经元的超结构变化.
主要方法:
- 死亡后的超结构形态测量研究.
- 对卫星微质细胞 (SatMg) 和尾状核头部相邻神经元的分析.
- 21名精神分裂症患者和20名健康对照患者之间的比较.
主要成果:
- 与老年对照人群相比,在年轻的精神分裂症患者中观察到微质密度增加.
- 精神分裂症的卫星微质体显示出较低的线粒体体积密度和数量,并增加了内分泌网膜真空面积.
- 精神分裂症的神经元表现出更大的体质,核,线粒体和内分泌网膜真空,与微质变化相关.
- 在精神分裂症患者中,神经元和微质细胞中增加的脂素颗粒与年龄和疾病持续时间相关.
结论:
- 在精神分裂症中,卫星微细胞与神经元相互作用的障碍可能源于内分泌网膜应激和微细胞中的线粒体缺陷.
- 这些微质细胞的改变,可能是由于慢性压力和激活,可能导致神经毒性,并导致精神分裂症的神经元衰老.
- 卫星微可能在精神分裂症中观察到的加速神经元衰老过程中发挥作用.
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