Xu Yuan-Qiao, Chen Yanjiao, Xing Jia-Xin, Yao Jun
School of Forensic Medicine, China Medical University, Shenyang, People's Republic of China.
Key Laboratory of Forensic Bio-Evidence Sciences, Shenyang, Liaoning Province, People's Republic of China.
Clin Epigenetics. 2025 Jan 24;17(1):13. doi: 10.1186/s13148-025-01820-4.
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.
丰富环境（EE）作为一种非药物干预措施，因其改善神经退行性疾病（NDs）的潜力而备受关注。本综述阐述了EE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、减轻炎症和提升认知表现方面的作用。我们讨论了EE作用的分子基础，包括对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，这些信号通路与神经保护和突触可塑性有关。此外，我们还审视了EE对表观遗传修饰和自噬的影响，这两个过程对ND发病机制至关重要。包括啮齿动物和大型动物在内的动物模型为EE的疾病修饰作用提供了见解，突出了其作为药物干预补充方法的潜力。总之，EE成为增强认知功能和减缓NDs进展的一种有前景的策略。
