p25对突触可塑性、学习和记忆的相反作用——好事过头反成坏事。

Antipodal effects of p25 on synaptic plasticity, learning, and memory--too much of a good thing is bad.

作者信息

LaFerla Frank M, Kitazawa Masashi

机构信息

Department of Neurobiology and Behavior, University of California, Irvine, 1109 Gillespie Neuroscience Research Facility, Irvine, California 92697, USA.

出版信息

Neuron. 2005 Dec 8;48(5):711-2. doi: 10.1016/j.neuron.2005.11.022.

DOI:10.1016/j.neuron.2005.11.022

PMID:16337907

Abstract

Elevated activity of the Cdk5/p25 complex has been implicated in the pathogenesis of Alzheimer's disease. The report by Fischer and colleagues in this issue of Neuron describes a dichotomous role for the activator protein p25 in synaptic plasticity, learning, and memory, whereby transient expression in transgenic mice produces beneficial effects, but prolonged expression is detrimental. This work demonstrates the complexity of Cdk5/p25 in neuronal function and shows that dysregulation of a factor involved in plasticity can cause neurodegeneration.

摘要

Cdk5/p25复合物活性升高与阿尔茨海默病的发病机制有关。Fischer及其同事在本期《神经元》杂志上发表的报告描述了激活蛋白p25在突触可塑性、学习和记忆中的双重作用，即转基因小鼠中的短暂表达产生有益效果，但长期表达则有害。这项研究证明了Cdk5/p25在神经元功能中的复杂性，并表明参与可塑性的一个因子失调可导致神经退行性变。