Neves Rodrigo C, Figueiredo Raquel C, Faria-Melibeu Adriana C
Laboratory Neurobiologia do Desenvolvimento, Instituto de Biologia, Universidade Federal Fluminense, R: Niterói, RJ, Brazil.
Curr Alzheimer Res. 2024;21(7):457-469. doi: 10.2174/0115672050348227241128095209.
Alzheimer's Disease (AD) is characterized by synapse loss and neurodegeneration, which leads to cognitive and psychiatric symptoms. Researchers worldwide have been studying therapeutic approaches aiming to induce plasticity and neuroprotection once AD has no cure and the existing treatments are limited. Environmental Enrichment (EE) is a change in housing conditions that promotes increased cognitive stimulus. Studies have demonstrated that EE acts as a plasticity modulator in several conditions and experimental models. In this review, we analyze and discuss the potential role of EE on plasticity modulation in different animal models but primarily on AD models. The data were extracted from the PubMed and ScienceDirect databases. The EE was shown to induce plasticity. LTP and behavior were enhanced in animals under different conditions, such as the AD model. The mechanisms were related to the glutamatergic system and excitatory/ inhibitory balance. Moreover, many studies have evidenced that EE promotes the upregulation of BDNF and the synaptic proteins SYN and PSD95. These data also suggest a neuroprotective function performed by EE in different contexts, such as aging and AD. Therefore, an enriched environment can be a target of new therapeutic approaches that aim to induce neuroplasticity and neuroprotection against AD.
阿尔茨海默病（AD）的特征是突触丧失和神经退行性变，这会导致认知和精神症状。由于AD无法治愈且现有治疗方法有限，世界各地的研究人员一直在研究旨在诱导可塑性和神经保护作用的治疗方法。环境富集（EE）是指居住条件的改变，可促进认知刺激的增加。研究表明，EE在多种情况和实验模型中可作为可塑性调节剂。在本综述中，我们分析并讨论了EE在不同动物模型中，尤其是在AD模型中对可塑性调节的潜在作用。数据从PubMed和ScienceDirect数据库中提取。结果显示，EE可诱导可塑性。在不同条件下，如AD模型中，动物的长时程增强（LTP）和行为得到增强。其机制与谷氨酸能系统以及兴奋性/抑制性平衡有关。此外，许多研究证明，EE可促进脑源性神经营养因子（BDNF）以及突触蛋白SYN和PSD95的上调。这些数据还表明，EE在不同背景下，如衰老和AD中发挥神经保护功能。因此，丰富的环境可以成为旨在诱导神经可塑性和针对AD的神经保护作用的新治疗方法的靶点。
