Splicing therapeutics for Alzheimer's disease

被引：6
|
作者：
Wasser, Catherine R. [1 ]
Herz, Joachim [1 ]
机构：
[1] Univ Texas SW Med Ctr Dallas, Dept Mol Genet, Ctr Translat Neurodegenerat Res, Dallas, TX 75390 USA
来源：
EMBO MOLECULAR MEDICINE | 2016年 / 8卷 / 04期
关键词：
D O I：
10.15252/emmm.201506067
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
The earliest clinical manifestation of Alzheimer's disease (AD) is cognitive impairment caused by synaptic dysfunction. ApoE4, the primary risk factor for late-onset AD, disrupts synaptic homeostasis by impairing synaptic ApoE receptor trafficking. Alternative splicing of ApoE receptor-2 (Apoer2) maintains synaptic homeostasis. In this issue, Hinrich etal (2016) show that Apoer2 splicing is impaired in human AD brains and murine AD models and that restoring normal splicing in the mouse rescues amyloid-induced cognitive defects.
引用
收藏
页码：308 / 310
页数：3
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