Alzheimer's disease (AD) and Parkinson's disease (PD) are neurodegenerative diseases (NDD) characterized by progressive degeneration of the central nervous system, and few medications are available to halt the progression of AD and PD. In the present study, an engineered strain MG136-pMG36e-GLP-1 was used to evaluate its neuroprotective effect on AD and PD mice, via the probiotics effects of Lactococcus lactis MG1363 and the constantly produced Glucagon-like peptide-1 (GLP-1) by the engineered strain. Our results indicated that oral administration of MG136-pMG36e-GLP-1 significantly reduced lipopolysaccharide (LPS)-induced memory impairment and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced motor dysfunction through the toll-like receptor4 (TLR4)/nuclear factor-kappa B (NFκB) and protein kinase B (AKT)/Glycogen synthase kinase-3β (GSK3β) signaling pathway. High-throughput sequencing results showed that MG1363-pMG36e-GLP-1 reduced the abundance of the pathogens Enterococcus, Proteus, and increased the abundance of the probiotics Akkermansia muciniphila. These results suggest that the engineered strain may be a new intervention for treating AD and PD by reducing the occurrence of neuroinflammation.

中文翻译：

---

GLP-1工程菌株对阿尔茨海默氏病和帕金森氏病小鼠模型的治疗作用。

阿尔茨海默氏病（AD）和帕金森氏病（PD）是神经退行性疾病（NDD），其特征是中枢神经系统进行性退行性变，很少有药物可以阻止AD和PD的发展。在本研究中，使用工程菌株MG136-pMG36e-GLP-1通过乳酸乳球菌MG1363和不断产生的胰高血糖素样肽1（GLP-1）的益生菌作用来评估其对AD和PD小鼠的神经保护作用。 ）。我们的结果表明，口服MG136-pMG36e-GLP-1可以显着减少脂多糖（LPS）引起的记忆障碍和1-甲基-4-苯基-1,2,3，6-四氢吡啶（MPTP）通过通行费样受体4（TLR4）/核因子-κB（NFκB）和蛋白激酶B（AKT）/糖原合酶激酶3β（GSK3β）信号传导途径诱导的运动功能障碍。高通量测序结果表明，MG1363-pMG36e-GLP-1降低了病原体肠球菌，变形杆菌的丰度，并增加了益生菌黏液阿克曼（Akkermansia muciniphila）的丰度。这些结果表明，工程菌株可能是通过减少神经炎症的发生而治疗AD和PD的新干预措施。