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在阿尔茨海默病发展过程中可能受损的替代神经回路。

Alternative neural circuitry that might be impaired in the development of Alzheimer disease.

作者信息

Avila Jesus, Perry George, Strange Bryan A, Hernandez Felix

机构信息

Neurobiology, Centro de Biologia Molecular Severo Ochoa (CSIC-UAM) Madrid, Spain ; Centro de Investigacion Biomedica en Red de Enfermedades Neurodegenerativas Madrid, Spain.

College of Sciences, The University of Texas at San Antonio San Antonio, TX, USA.

出版信息

Front Neurosci. 2015 Apr 23;9:145. doi: 10.3389/fnins.2015.00145. eCollection 2015.

DOI:10.3389/fnins.2015.00145
PMID:25954151
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4407584/
Abstract

It is well established that some individuals with normal cognitive capacity have abundant senile plaques in their brains. It has been proposed that those individuals are resilient or have compensation factors to prevent cognitive decline. In this comment, we explore an alternative mechanism through which cognitive capacity is maintained. This mechanism could involve the impairment of alternative neural circuitry. Also, the proportion of molecules such as Aβ or tau protein present in different areas of the brain could be important.

摘要

众所周知,一些认知能力正常的个体大脑中存在大量老年斑。有人提出,这些个体具有恢复力或具备防止认知衰退的补偿因素。在本评论中,我们探讨了一种维持认知能力的替代机制。这种机制可能涉及替代神经回路的损伤。此外,大脑不同区域中存在的诸如β淀粉样蛋白(Aβ)或 tau 蛋白等分子的比例可能也很重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c65c/4407584/8e4eb24bec5f/fnins-09-00145-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c65c/4407584/b1531f8cd53f/fnins-09-00145-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c65c/4407584/8e4eb24bec5f/fnins-09-00145-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c65c/4407584/b1531f8cd53f/fnins-09-00145-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c65c/4407584/8e4eb24bec5f/fnins-09-00145-g0002.jpg

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Subregional Density of Neurons, Neurofibrillary Tangles and Amyloid Plaques in the Hippocampus of Patients With Alzheimer's Disease.阿尔茨海默病患者海马体中神经元、神经原纤维缠结和淀粉样斑块的亚区域密度
Front Neuroanat. 2019 Dec 19;13:99. doi: 10.3389/fnana.2019.00099. eCollection 2019.

本文引用的文献

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The role of telomerase protein TERT in Alzheimer's disease and in tau-related pathology in vitro.端粒酶蛋白TERT在阿尔茨海默病及体外tau相关病理学中的作用。
J Neurosci. 2015 Jan 28;35(4):1659-74. doi: 10.1523/JNEUROSCI.2925-14.2015.
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Increased functional connectivity in the default mode network in mild cognitive impairment: a maladaptive compensatory mechanism associated with poor semantic memory performance.轻度认知障碍患者默认模式网络中功能连接性增加:一种与语义记忆表现不佳相关的适应不良性代偿机制。
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Glutamatergic regulation prevents hippocampal-dependent age-related cognitive decline through dendritic spine clustering.
谷氨酸能调节通过树突棘聚集预防海马体依赖性的年龄相关认知衰退。
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A common brain network links development, aging, and vulnerability to disease.一个常见的脑网络将发育、衰老和疾病易感性联系在一起。
Proc Natl Acad Sci U S A. 2014 Dec 9;111(49):17648-53. doi: 10.1073/pnas.1410378111. Epub 2014 Nov 24.
5
The Default Mode Network is functionally and structurally disrupted in amnestic mild cognitive impairment - a bimodal MEG-DTI study.默认模式网络在遗忘型轻度认知障碍中存在功能和结构破坏——一项双模态脑磁图-弥散张量成像研究
Neuroimage Clin. 2014 Sep 10;6:214-21. doi: 10.1016/j.nicl.2014.09.004. eCollection 2014.
6
Neural compensation in older people with brain amyloid-β deposition.脑淀粉样β蛋白沉积的老年人的神经代偿
Nat Neurosci. 2014 Oct;17(10):1316-8. doi: 10.1038/nn.3806. Epub 2014 Sep 14.
7
The impact of cognitive reserve on brain functional connectivity in Alzheimer's disease.认知储备对阿尔茨海默病脑功能连接的影响。
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Grid cells and cortical representation.网格细胞与皮层表象。
Nat Rev Neurosci. 2014 Jul;15(7):466-81. doi: 10.1038/nrn3766. Epub 2014 Jun 11.
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Cognitive reserve and Alzheimer's disease.认知储备与阿尔茨海默病。
Mol Neurobiol. 2015 Feb;51(1):187-208. doi: 10.1007/s12035-014-8720-y. Epub 2014 May 4.
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