真核延伸因子 2 激酶 (eEF2K) 在神经元可塑性、认知和阿尔茨海默病中的作用。
Roles of eukaryotic elongation factor 2 kinase (eEF2K) in neuronal plasticity, cognition, and Alzheimer disease.
机构信息
Department of Internal Medicine-Gerontology and Geriatric Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.
Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.
出版信息
J Neurochem. 2023 Jul;166(1):47-57. doi: 10.1111/jnc.15541. Epub 2021 Nov 27.
Abstract
Understanding the molecular signaling mechanisms underlying cognition and neuronal plasticity would provide insights into the pathogenesis of neuronal disorders characterized by cognitive syndromes such as Alzheimer disease (AD). Phosphorylation of the mRNA translational factor eukaryotic elongation factor 2 (eEF2) by its specific kinase eEF2K is critically involved in protein synthesis regulation. In this review, we discussed recent studies on the roles of eEF2K/eEF2 signaling in the context of regulation/dysregulation of cognitive function and synaptic plasticity. We specifically focus on the discussion of recent evidence indicating suppression of eEF2K signaling as a potential novel therapeutic avenue for AD and related dementias (ADRDs).
摘要
了解认知和神经元可塑性的分子信号机制将深入了解以认知综合征为特征的神经元疾病的发病机制，如阿尔茨海默病（AD）。其特定激酶 eEF2K 对 mRNA 翻译因子真核延伸因子 2（eEF2）的磷酸化在蛋白质合成调节中起着关键作用。在这篇综述中，我们讨论了 eEF2K/eEF2 信号在调节/失调认知功能和突触可塑性方面的最新研究。我们特别关注最近的证据表明抑制 eEF2K 信号作为 AD 和相关痴呆症（ADRDs）的一种潜在新的治疗途径的讨论。
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