Stress-induced tau phosphorylation: functional neuroplasticity or neuronal vulnerability?
Stress-induced tau phosphorylation: functional neuroplasticity or neuronal vulnerability?
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DOI：
10.3233/jad-2009-1153
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发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Rissman RA
中科院分区：
文献类型：
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作者：
Rissman RA
异常磷酸化的 tau 蛋白是阿尔茨海默病 (AD) 等神经退行性 tau 病病理学的关键组成部分。尽管 tau 磷酸化 (tau-P) 与疾病相关，但它也在神经可塑性中发挥着重要作用，例如海马体中为应对压力等环境挑战而发生的树突/突触重塑。为了界定神经可塑性和神经病理学之间的界限，研究试图描述应激诱导的 tau-P 涉及的范式、刺激和信号中间体。支持压力与 AD 相关的数据显示 AD 大脑中压力通路和肽的变化，以及流行病学数据表明压力暴露是 AD 的危险因素。在这篇综述中，将讨论应激诱导的 tau-P 是否可以用作检查功能性神经可塑性和神经元脆弱性之间关系的模型。
Abnormally phosphorylated tau protein is a key component of the pathology seen in neurodegenerative tauopathies, such as Alzheimer's disease (AD). Despite its association with disease, tau phosphorylation (tau-P) also plays an important role in neuroplasticity, such as dendritic/synaptic remodeling seen in the hippocampus in response to environmental challenges, such as stress. To define the boundaries between neuroplasticity and neuropathology, studies have attempted to characterize the paradigms, stimuli, and signaling intermediates involved in stress-induced tau-P. Supporting an involvement of stress in AD are data demonstrating alterations in stress pathways and peptides in the AD brain and epidemiological data implicating stress exposure as a risk factor for AD. In this review, the question of whether stress-induced tau-P can be used as a model for examining the relationship between functional neuroplasticity and neuronal vulnerability will be discussed.