GSK-3β and memory formation.
GSK-3β and memory formation.
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DOI：
10.3389/fnmol.2012.00047
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发表时间：
2012
影响因子：
4.8
通讯作者：
Takashima A
中科院分区：
文献类型：
--
作者：
Takashima A
在阿尔茨海默病（AD）中，tau过度磷酸化和神经原纤维缠结（NFT）的形成与痴呆症密切相关，这是该疾病的特征和早期特征。糖原合成酶激酶3β (GSK-3β)是tau蛋白正常和病理磷酸化的关键激酶。在患病状态下，过度磷酸化的tau沉积在nft中，nft的形成驱动了疾病的进程。GSK-3β也参与长期抑郁诱导，与tau相互作用抑制突触长期增强。强有力的证据表明GSK-3β的激活是导致老年和阿尔茨海默氏症中出现的记忆缺陷的原因。在这篇综述中，我们将重点关注GSK-3β在大脑功能中的作用，特别是在记忆维持方面。我们将检查人类和小鼠的研究，这些研究表明GSK-3β在记忆维持和记忆缺陷的最终发展中起作用。
In Alzheimer’s disease (AD), tau hyperphosphorylation and neurofibrillary tangle (NFT) formation are strongly associated with dementia, a characteristic and early feature of this disease. Glycogen synthase kinase 3β (GSK-3β) is a pivotal kinase in both the normal and pathological phosphorylation of tau. In the diseased state, hyperphosphorylated tau is deposited in NFTs, the formation of which, drive the disease process. GSK-3β which is also involved in long-term depression induction, interacts with tau to inhibit synaptic long-term potentiation. Strong lines of evidence suggest that the activation of GSK-3β is responsible for the memory deficits seen in both advanced age and AD. In this review, we will focus on the role of GSK-3β in brain function, particularly in memory maintenance. We will examine human and mouse studies which suggest a role for GSK-3β in memory maintenance and the eventual development of memory deficits.