Key Laboratory of Space Bioscience and Biotechnology, Engineering Research Center of Chinese Ministry of Education for Biological Diagnosis, Treatment and Protection Technology and Equipment, School of Life Sciences, Northwestern Polytechnical University, Xi'an, 710072, P. R. China.
J Nanobiotechnology. 2024 Sep 20;22(1):582. doi: 10.1186/s12951-024-02862-1.
Alzheimer's disease (AD) is a neurodegenerative disorder that can result in neurotoxicity and an imbalance in gut microbiota. Probiotics have been shown to play an important role in regulating the gut microbiota, but their viability and bioactivity are often compromised as they traverse the gastrointestinal tract, thereby reducing their efficacy and limiting their clinical utility.
In this work, layer-by-layer (LbL) encapsulation technology was used to encapsulate Lactiplantibacillus plantarum (LP) to improve the above shortcomings. Studies in APPswe/PS1dE9 (APP/PS1) transgenic mice show that LbL-encapsulated LP ((CS/SP)-LP) protects LP from gastrointestinal damage while (CS/SP)-LP treatment It improves brain neuroinflammation and neuronal damage in AD mice, reduces Aβ deposition, improves tau protein phosphorylation levels, and restores intestinal barrier damage in AD mice. In addition, post-synaptic density protein 95 (PSD-95) expression increased in AD mice after treatment, indicating enhanced synaptic plasticity. Fecal metabolomic and microbiological analyzes showed that the disordered intestinal microbiota composition of AD mice was restored and short-chain fatty acids (SCFAs) levels were significantly increased after (CS/SP)-LP treatment.
Overall, the above evidence suggests that (CS/SP)-LP can improve AD symptoms by restoring the balance of intestinal microbiota, and (CS/SP)-LP treatment will provide a new method to improve the symptoms of AD patients.
阿尔茨海默病(AD)是一种神经退行性疾病,可导致神经毒性和肠道微生物失衡。益生菌在调节肠道微生物群方面发挥着重要作用,但由于它们在穿过胃肠道时的生存能力和生物活性受到影响,从而降低了它们的疗效,并限制了它们的临床应用。
在这项工作中,采用层层(LbL)包封技术来包封植物乳杆菌(LP),以改善上述缺点。在 APPswe/PS1dE9(APP/PS1)转基因小鼠中的研究表明,LbL 包封的 LP[(CS/SP)-LP]在保护 LP 免受胃肠道损伤的同时,改善 AD 小鼠的脑神经炎症和神经元损伤,减少 Aβ 沉积,改善 tau 蛋白磷酸化水平,并恢复 AD 小鼠的肠道屏障损伤。此外,AD 小鼠经治疗后突触后密度蛋白 95(PSD-95)表达增加,表明突触可塑性增强。粪便代谢组学和微生物学分析表明,AD 小鼠紊乱的肠道微生物组成在(CS/SP)-LP 治疗后得到恢复,短链脂肪酸(SCFAs)水平显著升高。
总之,上述证据表明(CS/SP)-LP 通过恢复肠道微生物群的平衡来改善 AD 症状,(CS/SP)-LP 治疗将为改善 AD 患者的症状提供一种新方法。