阿尔茨海默病及其可能的进化起源:假设
James F Whitfield1, Kerry Rennie1, Balu Chakravarthy1
1Human Health Therapeutics, National Research Council, Ottawa, ON K1A 0R6, Canada.
Cells
|June 28, 2023
概括
阿尔茨海默病 (AD) 可能源于新皮层扩张和内皮层 (EC) 容量之间的进化不匹配. 针对粉样β oligomers (AβOs) 和Ca2+感应受体 (CaSRs) 的早期干预可以阻止AD的进展.
科学领域:
- 神经科学是一个神经科学.
- 进化生物学 进化生物学
- 病理学 病理学 病理学
背景情况:
- 人类新皮层扩张发生在进入海马的内腔皮层 (EC) 门户的补偿生长没有发生.
- 这种进化失衡可能解释了长寿人群中阿尔茨海默病 (AD) 的出现.
- 侧腔内皮层 (LEC) 上的年龄相关的处理应变可能会引发粉样β (Aβ) 病理.
研究的目的:
- 为了调查阿尔茨海默病 (AD) 的进化起源.
- 阐明脑内皮层 (EC) 和细胞蛋白 (PrPC) 在AD病变发生过程中的作用.
- 提出一种潜在的治疗策略来阻止AD.
主要方法:
- 对人类大脑发育的进化压力的分析.
- 检查了粉样β oligomers (AβOs),细胞蛋白 (PrPC) 和tau之间的分子相互作用.
- 研究Ca2+感应受体 (CaSRs) 在Aβ传播中的作用.
主要成果:
- 欧盟的有限能力与日益增加的新皮层数据作斗争,导致神经元应变和Aβ释放.
- 粉样β oligomers (AβOs) 与细胞蛋白 (PrPC) 结合,诱导陶过酸化和突触损伤.
- 由Ca2+感应受体 (CaSRs) 介导的粉样蛋白-β (Aβ) 生产,促进了AβO的传播.
结论:
- 阿尔茨海默氏病 (AD) 可能是由于进化不匹配而导致的连接病变故障.
- 细胞蛋白 (PrPC) 是AβOs诱导的神经退行症的核心.
- 结合AβOs和CaSR的治疗向可能提供一个有效的AD干预.
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