Lactobacillus paracasei PS23 Delays Progression of Age-Related Cognitive Decline in Senescence Accelerated Mouse Prone 8 (SAMP8) Mice

Huang, Shih Yi; Chen, Li Han; Wang, Mingfu; Hsu, Ching–Sheng; Chan, Ching Hung; Li, Jia Xian; Huang, Hui Yu

doi:10.3390/nu10070894

Cited by 69 publications

(75 citation statements)

References 57 publications

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“…The dose of LPPS23 used in the present study was obtained from previous studies [59–61, 75] and our pilot study. In the pilot study, the mice were given LPPS23 at either 1 × 10 8 or 1 × 10 9 CFU/mouse /day.…”

Section: Discussionmentioning

confidence: 99%

“…Eighteen female mice were divided into three groups each (n = 6), namely non-aging (sacrificed at week 0), control (fed for 12 weeks and treated with saline until an age of 28 weeks), and PS23 (fed for 12 weeks and treated with LPPS23 [1 × 10 9 CFU/mouse/day] until an age of 28 weeks) groups. The dose of LPPS23 was chosen based on our previous studies [75]. To ensure that the mice received live LPPS23, the bacteria were delivered by gavage performed by well-trained investigators.…”

Section: Methodsmentioning

confidence: 99%

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Lactobacillus paracasei PS23 decelerated age-related muscle loss by ensuring mitochondrial function in SAMP8 mice

Chen

Huang

et al. 2019

Aging

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Sarcopenia is a common impairment in the elderly population responsible for poor outcomes later in life; it can be caused by age-related alternations. Only a few strategies have been reported to reduce sarcopenia. Lactobacillus paracasei PS23 (LPPS23) has been reported to delay some age-related disorders. Therefore, here we investigated whether LPPS23 decelerates age-related muscle loss and its underlying mechanism. Female senescence-accelerated mouse prone-8 (SAMP8) mice were divided into three groups (n=6 each): non-aging (16-week-old), control (28-week-old), and PS23 (28-week-old) groups. The control and PS23 groups were given saline and LPPS23, respectively. We evaluated the effects of LPPS23 by analyzing body weight and composition, muscle strength, protein uptake, mitochondrial function, reactive oxygen species (ROS), antioxidant enzymes, and inflammation-related cytokines. LPPS23 significantly attenuated age-related decreases of muscle mass and strength. Compared to the control group, the non-aging and PS23 groups exhibited higher mitochondrial function, IL10, antioxidant enzymes, and protein uptake. Moreover, inflammatory cytokines and ROS were lower in the non-aging and PS23 groups than the control group. Taken together, LPPS23 extenuated sarcopenia progression during aging; this effect might have been enacted by preserving the mitochondrial function via reducing age-related inflammation and ROS and by retaining protein uptake in the SAMP8 mice.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Lactobacillus paracasei PS23 decelerated age-related muscle loss by ensuring mitochondrial function in SAMP8 mice

Chen

Huang

et al. 2019

Aging

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“…Furthermore, administration of Lactobacillus helveticus NS8 produced antidepressant effects in rats subjected to chronic restraint stress [10]. Oral ingestion of Lactobacillus paracasei in senescence accelerated mouse prone 8 (SAMP8) mice delayed age-related cognitive decline, possibly by preventing oxidation and inflammation [53]. Lactobacillus plantarum C29 treatment increased hippocampal BDNF and p-CREB expression and protected scopolamine-induced memory deficit in the Y-maze and Morris water maze tests [54].…”

Section: Discussionmentioning

confidence: 99%

Extracellular Vesicles Derived from Lactobacillus plantarum Increase BDNF Expression in Cultured Hippocampal Neurons and Produce Antidepressant-like Effects in Mice

Choi

Kim²,

Han

2019

Exp Neurobiol

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Gut microbiota play a role in regulating mental disorders, but the mechanism by which gut microbiota regulate brain function remains unclear. Gram negative and positive gut bacteria release membrane-derived extracellular vesicles (EVs), which function in microbiota-host intercellular communication. In the present study, we investigated whether Lactobacillus plantarum derived EVs ( L -EVs) could have a role in regulating neuronal function and stress-induced depressive-like behaviors. HT22 cells treated with the stress hormone glucocorticoid (GC; corticosterone) had reduced expression of Bdnf and Sirt1 , whereas L -EV treatment reversed GC-induced decreased expression of Bdnf and Sirt1 . The siRNA-mediated knockdown of Sirt1 in HT22 cells decreased Bdnf4 , a splicing variant of Bdnf , and Creb expression, suggesting that Sirt1 plays a role in L -EV-induced increase of BDNF and CREB expression. Mice exposed to restraint for 2-h daily for 14 days (CRST) exhibited depressive-like behaviors, and these CRST-treated mice had reduced expression of Bdnf and Nt4/5 in the hippocampus. In contrast, L -EV injection prior to each restraint treatment blocked the reduced expression of Bdnf and Nt4/5 , and stress-induced depressive-like behaviors. Furthermore, L -EV treatment in CRST-treated mice also rescued the reduced expression of Bdnf , and blocked stress-induced depressive-like behaviors. These results suggest that Lactobacillus derived EVs can change the expression of neurotropic factors in the hippocampus and afford antidepressant-like effects in mice with stress-induced depression.

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“…This evidence was obtained from experiments with the SAMP8 mouse, which is a model of age-related cognitive decline that exhibits early-stage neurodegeneration with impaired learning and memory abilities [26]. SAMP8 mice start aging rapidly at 4 months of age, although at younger ages they are identical to SAMR1 mice [27]. Therefore, we studied aged SAMP8 mice at 10 months old that had begun FA treatments at 4 months old.…”

Section: Discussionmentioning

confidence: 99%

Folic acid delays age-related cognitive decline in senescence-accelerated mouse prone 8: alleviating telomere attrition as a potential mechanism

Lv¹,

Wang²,

Wang³

et al. 2019

Aging

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The occurrence of telomere attrition in brain may cause senescence and death of neurons, leading to cognitive decline. Folic acid (FA) has been reported to improve cognitive performance in mild cognitive impairment; however, its association with telomere remains unclear. The study aimed to investigate if alleviation of telomere attrition by FA supplementation could act as a potential mechanism to delay age-related cognitive decline in senescence-accelerated mouse prone 8 (SAMP8). Aged SAMP8 mice were assigned to four treatment groups: FAdeficient diet (FA-D) group, FA-normal diet (FA-N) group, low FA-supplemented diet (FA-L) group and high FAsupplemented diet (FA-H) group. There was also an age-matched senescence-accelerated mouse resistant 1 (SAMR1) control group (Con-R), and a young SAMP8 control group (Con-Y). The results demonstrated that FA supplementation delayed age-related cognitive decline and neurodegeneration in SAMP8 mice. Importantly, this effect could be attributed to the alleviated telomere attrition, which might be interpreted by the decreased levels of reactive oxygen species. Additionally, improved telomere integrity stimulated mitochondrial function via telomere-p53-mithondria pathway, consequently delayed neuronal degeneration. In conclusion, we demonstrate that FA supplementation delays age-related neurodegeneration and cognitive decline in SAMP8 mice, in which alleviated telomere attrition could serve as one influential factor in the process.

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Lactobacillus paracasei PS23 Delays Progression of Age-Related Cognitive Decline in Senescence Accelerated Mouse Prone 8 (SAMP8) Mice

Cited by 69 publications

References 57 publications

Lactobacillus paracasei PS23 decelerated age-related muscle loss by ensuring mitochondrial function in SAMP8 mice

Lactobacillus paracasei PS23 decelerated age-related muscle loss by ensuring mitochondrial function in SAMP8 mice

Extracellular Vesicles Derived from Lactobacillus plantarum Increase BDNF Expression in Cultured Hippocampal Neurons and Produce Antidepressant-like Effects in Mice

Folic acid delays age-related cognitive decline in senescence-accelerated mouse prone 8: alleviating telomere attrition as a potential mechanism

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