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小鼠模型中的环境富集及其向改善阿尔茨海默病状况的人为因素的转化

Environmental Enrichment in Murine Models and Its Translation to Human Factors Improving Conditions in Alzheimer Disease.

作者信息

Colavitta M F, Grasso L, Barrantes F J

机构信息

Francisco J. Barrantes, Laboratory of Molecular Neurobiology, Biomedical Research Institute (BIOMED), UCA-CONICET. Av. Alicia Moreau de Justo, C1107AAZ Buenos Aires, Argentina,

出版信息

J Prev Alzheimers Dis. 2023;10(2):287-300. doi: 10.14283/jpad.2023.5.

DOI:10.14283/jpad.2023.5
PMID:36946456
Abstract

With the aging of the world population, there has been a notable increase in the incidence of Alzheimer disease (AD), the most prevalent neurodegenerative disease affecting the elderly. Several studies have reported a delay in the onset of AD symptoms and age-related cognitive dysfunction upon changes to a healthier lifestyle. These positive adjustments find support in the cognitive reserve hypothesis, which holds that the ability to defer disease inception and protect cognitive performance is related to healthier lifestyle habits such as cognitive and physical activity, social engagement, and sensorial stimulation. These lifestyle habits can be compounded under the umbrella of the environmental enrichment (EE) paradigm. The mechanisms underlying EE's capacity to modulate disease expression remain unclear. Since ethical and methodological considerations rule out direct analysis of such changes in the human brain, researchers have resorted to animal models to carry out in-depth characterizations of post-EE structural and functional brain modifications using a variety of behavioral, electrophysiological, genetic, biochemical, and biophysical approaches. Moreover, given the shorter lifespan of animals compared to humans, it is possible to address the effects of aging in control and AD models. In this review we analyze and classify EE data from studies using AD murine models and compare the setup variables employed. We also delve into various aspects of neuroplasticity, under the posit that this property is the key mechanistic process underlying the benefits of EE in both animal and human subjects.

摘要

随着世界人口老龄化,阿尔茨海默病(AD)的发病率显著上升,AD是影响老年人的最常见神经退行性疾病。多项研究报告称,改变为更健康的生活方式后,AD症状和与年龄相关的认知功能障碍的发病会延迟。这些积极调整在认知储备假说中得到支持,该假说认为推迟疾病发作和保护认知表现的能力与更健康的生活习惯有关,如认知和体育活动、社交参与以及感官刺激。这些生活习惯可以在环境富集(EE)范式的框架下综合起来。EE调节疾病表现的潜在机制尚不清楚。由于伦理和方法学上的考虑排除了对人类大脑此类变化的直接分析,研究人员已诉诸动物模型,使用各种行为、电生理、遗传、生化和生物物理方法对EE后大脑的结构和功能改变进行深入表征。此外,鉴于动物的寿命比人类短,有可能在对照和AD模型中研究衰老的影响。在这篇综述中,我们分析并分类了使用AD小鼠模型的研究中的EE数据,并比较了所采用的设置变量。我们还深入探讨了神经可塑性的各个方面,假定这一特性是EE对动物和人类受试者有益的关键机制过程。

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