摘要
Recent reports on experimental models of neurodegeneration in mice have strengthened the notion that environmental enrichment (EE) is beneficial, in terms of delayed onset and progression, to a variety of neurodegenerative diseases. These studies also revealed interesting mechanistic understandings as to how EE might function. While it is generally assumed that EE elicits transcriptional and translational events that on the whole tend to be neuroprotective and neurogenic, fairly specific changes that appear to target the underlying pathological causes of disease in these various mouse models have been noted. These include a possible restoration of brain-derived neurotrophic factor striatal transport in the R6/1 Huntington’s mice and an elevation in the levels of amyloid-degrading enzyme neprilysin in the APPswe/PS1ΔE9 Alzheimic mice. An elevation in glial-derived neurotrophic factor coupled to a reduction in dopamine transporter may underlie beneficial effects in mice with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinsonian symptoms. How all these findings would translate to disease settings in human patients are unclear, but they do provide useful leads for further clinical and paraclinical investigations.
摘要译文
最近关于小鼠神经退行性实验模型的报道强化了环境浓缩（EE）在延迟发作和进展方面是有益的概念，对各种神经变性疾病的影响这些研究还揭示了有关EE如何运作的有趣的机械理解虽然通常假定EE引起转录和翻译事件，其总体趋向于具有神经保护和神经源性，已经注意到在这些各种小鼠模型中看来以疾病的潜在病理原因为目标的相当具体的变化在R6 / 1亨廷顿小鼠中脑源性神经营养因子纹状体运输的变化和APPswe / PS1螖E9阿尔茨海默氏小鼠中淀粉样蛋白降解酶血浆蛋白酶水平的升高与多巴胺转运蛋白减少偶联的神经胶质衍生的神经营养因子的升高可能是用1-甲基-4-苯基-1,2,3,4-四氢吡啶6-四氢吡啶诱导的帕金森病症状。所有这些发现将转化为人类患者的疾病设置尚不清楚，但它们为进一步的临床和临床研究提供了有用的线索
Lingzhi Li; Bor Luen Tang. Environmental enrichment and neurodegenerative diseases[J]. Biochemical and Biophysical Research Communications, 2005,334(2): 293–297