| First Author | Huang HJ | Year | 2021 |
| Journal | BMC Complement Med Ther | Volume | 21 |
| Issue | 1 | Pages | 259 |
| PubMed ID | 34627204 | Mgi Jnum | J:368891 |
| Mgi Id | MGI:8215675 | Doi | 10.1186/s12906-021-03426-8 |
| Citation | Huang HJ, et al. (2021) Lactobacillus plantarum PS128 prevents cognitive dysfunction in Alzheimer's disease mice by modulating propionic acid levels, glycogen synthase kinase 3 beta activity, and gliosis. BMC Complement Med Ther 21(1):259 |
| abstractText | BACKGROUND: According to recent evidence, psychobiotics exert beneficial effects on central nervous system-related diseases, such as mental disorders. Lactobacillus plantarum PS128 (PS128), a novel psychobiotic strain, improves motor function, depression, and anxiety behaviors. However, the psychobiotic effects and mechanisms of PS128 in Alzheimer's disease (AD) remain to be explored. OBJECTIVES: The goal of the current study was to evaluate the beneficial effects of PS128 and to further elucidate its mechanism in AD mice. METHODS: PS128 (10(10) colony-forming unit (CFU)/ml) was administered via oral gavage (o.g.) to 6-month-old male wild-type B6 and 3 x Tg-AD mice (harboring the PS1M146V, APPswe and TauP30IL transgenes) that received an intracerebroventricular injection of streptozotocin (icv-STZ, 3 mg/kg) or vehicle (saline) for 33 days. After serial behavioral tests, fecal short-chain fatty acid levels and AD-related pathology were assessed in these mice. RESULTS: Our findings show that intracerebroventricular injection of streptozotocin accelerated cognitive dysfunction associated with increasing levels of glycogen synthase kinase 3 beta (GSK3beta) activity, tau protein phosphorylation at the T231 site (pT231), amyloid-beta (Abeta) deposition, amyloid-beta protein precursor (AbetaPP), beta-site AbetaPP-cleaving enzyme (BACE1), gliosis, fecal propionic acid (PPA) levels and cognition-related neuronal loss and decreasing postsynaptic density protein 95 (PSD95) levels in 3 x Tg-AD mice. PS128 supplementation effectively prevented the damage induced by intracerebroventricular injection of streptozotocin in 3 x Tg-AD mice. CONCLUSIONS: Based on the experimental results, intracerebroventricular injection of streptozotocin accelerates the progression of AD in the 3 x Tg-AD mice, primarily by increasing the levels of gliosis, which were mediated by the propionic acid and glycogen synthase kinase 3 beta pathways. PS128 supplementation prevents damage induced by intracerebroventricular injection of streptozotocin by regulating the propionic acid levels, glycogen synthase kinase 3 beta activity, and gliosis in 3 x Tg-AD mice. Therefore, we suggest that PS128 supplementation is a potential strategy to prevent and/or delay the progression of AD. |
