益生素缺乏驱动糖尿病相关的认知功能障碍,诱导微质介导的突触损失
Jiaxuan Jiang1,2, Pengzi Zhang1,2, Yue Yuan1,2
1Department of Endocrinology, Endocrine and Metabolic Disease Medical Center, Affiliated Hospital of Medical School, Nanjing Drum Tower Hospital, Nanjing University, Nanjing, China.
Journal of neuroinflammation
|November 15, 2024
概括
降低的益生素 (PRL) 水平与2型糖尿病 (T2DM) 的认知衰退和海马损伤有关. 恢复PRL水平可以改善认知功能,并减少糖尿病小鼠的突触损失.
科学领域:
- 神经内分泌学神经内分泌学
- 代谢障碍 代谢障碍 代谢障碍
- 认知神经科学是一种认知神经科学.
背景情况:
- 糖尿病相关的认知功能障碍涉及早期的海马突触损失.
- 激素,特别是垂体激素,在突触调节中发挥作用.
- 下垂体激素与糖尿病认知衰退之间的关系需要进一步研究.
研究的目的:
- 探索下垂体激素与2型糖尿病 (T2DM) 的认知衰退之间的关联.
- 调查益生菌 (PRL) 在糖尿病相关认知障碍和海马病理学中的作用.
主要方法:
- 在744名T2DM患者的临床研究中,对垂体激素,认知和MRI进行了评估.
- 糖尿病小鼠模型 (HFD养) 具有动态饮食干预措施.
- 在淘汰赛小鼠 (PRL,神经PRLR,微质PRLR) 和注入PRL的小鼠中评估认知表现和海马病理学.
主要成果:
- 降低PRL水平与T2DM患者的认知障碍和海马体损伤相关.
- 在糖尿病小鼠中,降低PRL之前有突触损失和认知衰退.
- 微质PRL受体 (PRLR) 淘汰,而不是神经元,导致突触损失和认知障碍.
- 在糖尿病小鼠中,PRL输液减轻了微质介导的突触损失,并改善了认知功能.
结论:
- 降低的益生素 (PRL) 水平有助于T2DM的认知功能障碍和海马体突触损失.
- 该机制涉及由于PRL降低而增加的微质介导突触吞.
- 恢复PRL水平显示了对糖尿病认知缺陷和突触损伤的治疗潜力.
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