Regulation of tau phosphorylation in Alzheimer's disease
Regulation of tau phosphorylation in Alzheimer's disease
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DOI：
10.1111/j.1749-6632.1996.tb34408.x
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发表时间：
1996-01-01
期刊：
影响因子：
--
通讯作者：
Lee, VMY
中科院分区：
文献类型：
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作者：
Lee, VMY
阿尔茨海默病（Alzheimer's disease，AD）是一种以进行性认知障碍、大量淀粉样蛋白或老年斑（senile plaque，SP）和神经元缠结（neuroendocrine tangles，NFT）的积累以及AD脑内神经元大量丢失为特征的老年异质性痴呆症。事实上，在慢性进行性痴呆患者中AD的安全诊断需要死后大脑中大量SP和NFT的证据。虽然细胞外斑块中纤维状淀粉样蛋白或A β肽的沉积和富含tau的神经元内NFT的积累并不仅限于AD，但在选定的端脑区域中富含tau的神经元病变的负担与AD中的痴呆之间存在密切相关性。由于过度磷酸化的tau蛋白形成的神经病变可能会损害AD脑中神经元的功能和活力，本文综述了AD中调节tau蛋白磷酸化状态的机制。
Alzheimer's disease (AD) is a heterogeneous dementing disorder of the elderly that is characterized by progressive cognitive impairments and the accumulation of abundant amyloid or senile plaques (SPs) and neurofibrillary tangles (NFTs) as well as the massive loss of neurons in the AD brain. Indeed, a secure diagnosis of AD in patients with a chronic progressive dementia requires evidence of numerous SPs and NFTs in the postmortem brain. Although the deposition of fibrillar amyloid or A beta-peptides in extracellular plaques and the accumulation of tau-rich intraneuronal NFTs are not restricted exclusively to AD, there is a close correlation between the burden of tau-rich neurofibrillary lesions in selected telencephalic regions of the brain and the dementia in AD. Since the formation of neurofibrillary lesions from hyperphosphorylated tau proteins may compromise the function and viability of neurons in the AD brain, this review summarizes recent insights into mechanisms that regulate the phosphorylation state of tau in AD.