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Updated: Sep 12, 2025

SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry
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SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry

Published on: January 6, 2017

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阿尔茨海默病风险基因SORL1是激发性神经元功能的调节者

C Andrew Williams1,2, Shannon E Rose1,2, Vera Stamenkovic3

  • 1Department of Laboratory Medicine and Pathology, University of Washington School of Medicine, Seattle, WA, USA.

bioRxiv : the preprint server for biology
|August 6, 2025
PubMed
概括

在阿尔茨海默氏病 (AD) 模型中,SORL1蛋白质的损失会损害突触功能和可塑性. 这种功能障碍源于改变的蛋白质贩运,而不是粉样β,突出显示了AD治疗的SORL1-复原体通路.

关键词:
阿尔茨海默氏症是阿尔茨海默氏症的一种疾病.氨基酸ββ类.这是内分体贩运.谷氨酸受体的受体是什么神经元过度活动.复原蛋白是复原体中的一个.这就是SORL1的原因.索拉拉 (SORLA) 是一个突触突触是一个突触突触.突触性可塑性 突触性可塑性由iPSC衍生的神经元.

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