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本文引用的文献

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Harm avoidance and cerebral infarction.避免伤害与脑梗死
Neuropsychology. 2014 Mar;28(2):305-11. doi: 10.1037/neu0000022. Epub 2013 Dec 23.
2
TDP-43 pathology, cognitive decline, and dementia in old age.老年 TDP-43 病理学、认知能力下降与痴呆。
JAMA Neurol. 2013 Nov;70(11):1418-24. doi: 10.1001/jamaneurol.2013.3961.
3
A two-decade comparison of prevalence of dementia in individuals aged 65 years and older from three geographical areas of England: results of the Cognitive Function and Ageing Study I and II.英格兰三个地区 65 岁及以上人群痴呆患病率 20 年对比:认知功能与老龄化研究 I 和 II 的结果。
Lancet. 2013 Oct 26;382(9902):1405-12. doi: 10.1016/S0140-6736(13)61570-6. Epub 2013 Jul 17.
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Genetic susceptibility for Alzheimer disease neuritic plaque pathology.阿尔茨海默病神经原纤维缠结病理的遗传易感性。
JAMA Neurol. 2013 Sep 1;70(9):1150-7. doi: 10.1001/jamaneurol.2013.2815.
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Comparative lipidomics of mouse brain exposed to enriched environment.富氧环境暴露对小鼠大脑脂质组学的比较研究。
J Lipid Res. 2013 Oct;54(10):2687-96. doi: 10.1194/jlr.M038075. Epub 2013 Jul 6.
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Life-span cognitive activity, neuropathologic burden, and cognitive aging.寿命期认知活动、神经病理学负担与认知老化。
Neurology. 2013 Jul 23;81(4):314-21. doi: 10.1212/WNL.0b013e31829c5e8a. Epub 2013 Jul 3.
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Twenty-year changes in dementia occurrence suggest decreasing incidence in central Stockholm, Sweden.二十年来痴呆症发病率的变化表明瑞典斯德哥尔摩中心的发病率正在下降。
Neurology. 2013 May 14;80(20):1888-94. doi: 10.1212/WNL.0b013e318292a2f9. Epub 2013 Apr 17.
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An inflection point in gene discovery efforts for neurodegenerative diseases: from syndromic diagnoses toward endophenotypes and the epigenome.神经退行性疾病基因发现工作的转折点:从综合征诊断到表型和表观基因组。
JAMA Neurol. 2013 Jun;70(6):719-26. doi: 10.1001/jamaneurol.2013.275.
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Neural reserve, neuronal density in the locus ceruleus, and cognitive decline.神经储备、蓝斑神经元密度与认知衰退。
Neurology. 2013 Mar 26;80(13):1202-8. doi: 10.1212/WNL.0b013e3182897103. Epub 2013 Mar 13.
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Intrinsic connectivity networks and personality: the temperament dimension harm avoidance moderates functional connectivity in the resting brain.内在连接网络与人格:气质维度中的抑制回避调节静息态大脑的功能连接。
Neuroscience. 2013 Jun 14;240:98-105. doi: 10.1016/j.neuroscience.2013.02.056. Epub 2013 Mar 4.

认知和社会生活方式:与晚年神经病理学和认知的关系。

Cognitive and social lifestyle: links with neuropathology and cognition in late life.

机构信息

Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA,

出版信息

Acta Neuropathol. 2014 Jan;127(1):137-50. doi: 10.1007/s00401-013-1226-2. Epub 2013 Dec 20.

DOI:10.1007/s00401-013-1226-2
PMID:24356982
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4054865/
Abstract

Many studies report an association of cognitive and social experiential factors and related traits with dementia risk. Further, many clinical-pathologic studies find a poor correspondence between levels of neuropathology and the presence of dementia and level of cognitive impairment. The poor correspondence suggests that other factors contribute to the maintenance or loss of cognitive function, with factors associated with the maintenance of function referred to as neural or cognitive reserve. This has led investigators to examine the associations of cognitive and social experiential factors with neuropathology as a first step in disentangling the complex associations between these experiential risk factors, neuropathology, and cognitive impairment. Despite the consistent associations of a range of cognitive and social lifestyle factors with cognitive decline and dementia risk, the extant clinical-pathologic data find only a single factor from one cohort, linguistic ability, related to AD pathology. Other factors, including education, harm avoidance, and emotional neglect, are associated with cerebrovascular disease. Overall, the associations are weak. Some factors, such as education, social networks, and purpose in life, modify the relation of neuropathology to cognition. Finally, some factors such as cognitive activity appear to bypass known pathologies altogether suggesting a more direct association with biologic indices that promote person-specific differences in reserve and resilience. Future work will first need to replicate findings across more studies to ensure the veracity of the existing data. Second, effort is needed to identify the molecular substrates of neural reserve as potential mediators of the association of lifestyle factors with cognition.

摘要

许多研究报告表明认知和社会经验因素及相关特征与痴呆风险之间存在关联。此外,许多临床病理研究发现,神经病理学的水平与痴呆的存在和认知障碍的水平之间存在较差的对应关系。这种较差的对应关系表明,其他因素也有助于维持或丧失认知功能,与维持功能相关的因素被称为神经或认知储备。这促使研究人员检查认知和社会经验因素与神经病理学之间的关联,作为厘清这些经验风险因素、神经病理学和认知障碍之间复杂关联的第一步。尽管一系列认知和社会生活方式因素与认知衰退和痴呆风险之间存在一致的关联,但现有的临床病理数据仅在一个队列中发现了一个与 AD 病理相关的单一因素,即语言能力。其他因素,包括教育、回避伤害和情感忽视,与脑血管疾病有关。总的来说,这些关联是微弱的。一些因素,如教育、社交网络和生活目标,会改变神经病理学与认知之间的关系。最后,一些因素,如认知活动,似乎完全绕过了已知的病理,这表明与促进个体差异的储备和韧性的生物学指标有更直接的关联。未来的工作首先需要在更多的研究中复制这些发现,以确保现有数据的真实性。其次,需要努力确定神经储备的分子基础,作为生活方式因素与认知相关的潜在中介。