Transcriptional regulation of APP by apoE: To boldly go where no isoform has gone before: ApoE, APP transcription and AD: Hypothesised mechanisms and existing knowledge gaps.
Transcriptional regulation of APP by apoE: To boldly go where no isoform has gone before: ApoE, APP transcription and AD: Hypothesised mechanisms and existing knowledge gaps.
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DOI：
10.1002/bies.201700062
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发表时间：
2017-09
期刊：
影响因子：
--
通讯作者：
Koo EH
中科院分区：
文献类型：
--
作者：
Lee LC;Goh MQL;Koo EH
阿尔茨海默病（AD）是最常见的痴呆症，逐渐破坏大脑网络，损害记忆，语言和认知。虽然淀粉样蛋白假说仍然是解释AD病理生理学的主要机制，但抗淀粉样蛋白治疗策略尚未转化为有用的疗法，这表明淀粉样蛋白β-蛋白及其前体，淀粉样蛋白前体蛋白（APP）只是疾病级联的一部分。此外，AD的风险可以由许多因素调节，最有影响力的是载脂蛋白E（apoE）的ε4同种型。最近的一项研究报道了apoE对APP的一种新的异构体依赖性转录调控。这些有趣的新结果增加了已提出的解释apoE 4如何增加AD风险的无数机制，突出了apoE和AD病理生理学以及疾病本身的复杂性。
Alzheimer's disease (AD) is the most common form of dementia, gradually disrupting the brain network to impair memory, language, and cognition. While the amyloid hypothesis remains the leading proposed mechanism to explain AD pathophysiology, anti-amyloid therapeutic strategies have yet to translate into useful therapies, suggesting that amyloid β-protein and its precursor, the amyloid precursor protein (APP) are but a part of the disease cascade. Further, risk of AD can be modulated by a number of factors, the most impactful being the ε4 isoform of apolipoprotein E (apoE). A recent study reported a novel isoform-dependent transcriptional regulation of APP by apoE. These interesting new results add to the myriad of mechanisms that have been proposed to explain how apoE4 enhances AD risk, highlighting the complexities of not only apoE and AD pathophysiology, but also of disease itself.
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影响因子：
4.3
作者：
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