Relationship between enriched environment and neurodegeneration: a review from mechanism to therapy.

IF 4.8 2区 医学 Q1 GENETICS & HEREDITY
Yuan-Qiao Xu, Yanjiao Chen, Jia-Xin Xing, Jun Yao
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引用次数: 0

Abstract

Enriched environment (EE), as a non-pharmacological intervention, has garnered considerable attention for its potential to ameliorate neurodegenerative diseases (NDs). This review delineated the impact of EE on the biological functions associated with NDs, emphasizing its role in enhancing neural plasticity, reducing inflammation, and bolstering cognitive performance. We discussed the molecular underpinnings of the effects of EE, including modulation of key signaling pathways such as extracellular regulated kinase 1/2 (ERK1/2), mitogen-activated protein kinases (MAPK), and AMPK/SIRT1, which were implicated in neuroprotection and synaptic plasticity. Additionally, we scrutinized the influence of EE on epigenetic modifications and autophagy, processes pivotal to ND pathogenesis. Animal models, encompassing both rodents and larger animals, offer insights into the disease-modifying effects of EE, underscoring its potential as a complementary approach to pharmacological interventions. In summary, EE emerges as a promising strategy to augment cognitive function and decelerate the progression of NDs.

富集环境与神经退行性变的关系:从机制到治疗的综述。
富集环境(EE)作为一种非药物干预手段,因其改善神经退行性疾病(NDs)的潜力而受到广泛关注。这篇综述描述了情感表达对与NDs相关的生物学功能的影响,强调了其在增强神经可塑性、减少炎症和增强认知能力方面的作用。我们讨论了EE影响的分子基础,包括关键信号通路的调节,如细胞外调节激酶1/2 (ERK1/2)、丝裂原活化蛋白激酶(MAPK)和AMPK/SIRT1,它们与神经保护和突触可塑性有关。此外,我们仔细研究了EE对表观遗传修饰和自噬的影响,这是ND发病的关键过程。动物模型,包括啮齿类动物和大型动物,提供了对情感表达的疾病改善作用的见解,强调了其作为药物干预补充方法的潜力。综上所述,情感表达是增强认知功能和减缓NDs进展的一种有前景的策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
自引率
5.30%
发文量
150
期刊介绍: Clinical Epigenetics, the official journal of the Clinical Epigenetics Society, is an open access, peer-reviewed journal that encompasses all aspects of epigenetic principles and mechanisms in relation to human disease, diagnosis and therapy. Clinical trials and research in disease model organisms are particularly welcome.
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