酶激活之前,并导致纠
Alix de Calignon1, Leora M Fox, Rose Pitstick
1MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Alzheimer's Disease Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Nature
|April 2, 2010
概括
酶激活,而不是神经纤维状结 (NFT),在阿尔茨海默病模型中启动病理. 这一发现表明可溶性种,而不是,驱动神经退行,提供新的治疗点.
科学领域:
- 神经科学是一个神经科学.
- 分子生物学分子生物学
- 病理学 病理学 病理学
背景情况:
- 验尸研究将神经纤维状结 (NFT) 与阿尔茨海默病 (AD) 和前性痴呆中的神经元死亡联系起来.
- NFT与酶激活和亡有关,这表明结会导致神经退行.
研究的目的:
- 在体内调查酶激活和NFT形成之间的时间关系.
- 阐明酶分裂的在启动病理和神经退行症中的作用.
主要方法:
- 在活体多光子成像中活着的tau转基因小鼠 (Tg4510菌株).
- 对酶激活和NFT形成的观察.
- 在野生类型的小鼠中引入野生类型的4重复的 (tau-4R) 和裂的结构.
主要成果:
- 卡斯帕斯激活在NFT形成之前数小时到几天.
- 新的NFT在一天内形成,神经元通过抑制的酶活动生存下来.
- 酶激活,突断和聚合是由tau-4R引入引发的.
- 卡斯帕斯分裂的陶氏仿真诱导聚合物,纠结表位和内源性陶氏招募.
结论:
- 一种新型模型提出,酶激活启动分裂,导致NFT形成.
- NFT可能是"脱离急性神经元死亡的途径",纠性神经元的寿命较长.
- 溶解的物种,而不是纤维状,可能是神经退行的主要毒剂.
相关概念视频
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