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金属离子在唐氏综合征认知能力下降中的作用。

Role of metal ions in the cognitive decline of Down syndrome.

机构信息

Oxidation Biology Unit, Florey Institute of Neuroscience and Mental Health Parkville, VIC, Australia.

Department of Biochemistry, Monash University Clayton, VIC, Australia.

出版信息

Front Aging Neurosci. 2014 Jun 23;6:136. doi: 10.3389/fnagi.2014.00136. eCollection 2014.

DOI:10.3389/fnagi.2014.00136
PMID:25002847
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4066992/
Abstract

Down syndrome (DS), caused by trisomy of whole or part of chromosome 21 is the most common mental impairment. All people with DS suffer from cognitive decline and develop Alzheimer's disease (AD) by the age of 40. The appearance of enlarged early endosomes, followed by Amyloid βpeptide deposition, the appearance of tau-containing neurofibrillary tangles and basal forebrain cholinergic neuron (BFCN) degeneration are the neuropathological characteristics of this disease. In this review we will examine the role of metal ion dyshomeostasis and the genes which may be involved in these processes, and relate these back to the manifestation of age-dependent cognitive decline in DS.

摘要

唐氏综合征(DS)是由 21 号染色体全部或部分三体引起的,是最常见的智力障碍。所有唐氏综合征患者都会出现认知能力下降,并在 40 岁前发展为阿尔茨海默病(AD)。早期内体增大,随后β淀粉样肽沉积、含tau 的神经原纤维缠结出现以及基底前脑胆碱能神经元(BFCN)退化是这种疾病的神经病理学特征。在这篇综述中,我们将研究金属离子动态平衡紊乱的作用以及可能涉及这些过程的基因,并将这些与 DS 中与年龄相关的认知能力下降的表现联系起来。

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本文引用的文献

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Phosphorylation of amyloid precursor protein at threonine 668 is essential for its copper-responsive trafficking in SH-SY5Y neuroblastoma cells.淀粉样前体蛋白在苏氨酸 668 处的磷酸化对于其在 SH-SY5Y 神经母细胞瘤细胞中的铜响应性转运是必不可少的。
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Increased expression of the glucose-responsive gene, RCAN1, causes hypoinsulinemia, β-cell dysfunction, and diabetes.葡萄糖反应基因 RCAN1 的表达增加会导致胰岛素分泌不足、β 细胞功能障碍和糖尿病。
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The metal theory of Alzheimer's disease.阿尔茨海默病的金属理论。
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Tau deficiency induces parkinsonism with dementia by impairing APP-mediated iron export.tau 蛋白缺失通过损害 APP 介导体铁输出而诱导帕金森病伴痴呆。
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Metal binding dictates conformation and function of the amyloid precursor protein (APP) E2 domain.金属结合决定淀粉样前体蛋白 (APP) E2 结构域的构象和功能。
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Modulation of neuronal signal transduction and memory formation by synaptic zinc.突触锌对神经元信号转导和记忆形成的调节作用。
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