Long-Term Diet Supplementation with Lactobacillus paracasei K71 Prevents Age-Related Cognitive Decline in Senescence-Accelerated Mouse Prone 8

Corpuz, Henry M.; Ichikawa, Saki; Arimura, Misa; Mihara, Toshihiro; Kumagai, Takehisa; Mitani, Takahiko; Nakamura, Soichiro; Katayama, Shigeru

doi:10.3390/nu10060762

Cited by 52 publications

(44 citation statements)

References 33 publications

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“…Similarly, Kadry & Megeed (2018) found that Lactobacillus could effectively inhibit the reduction of BDNF induced by cadmium chloride in the hippocampus of mice. Moreover, Corpuz et al (2018) reported that Lactobacillus paracasei K71 prevents age-related cognitive decline in senescence-accelerated mouse prone 8 by increasing the protein expression of BDNF and the phosphorylation of CREB in the hippocampus. Neuroplasticity also needs the regulation of NCAM (Seidenfaden, Krauter & Hildebrandt, 2006) and the stimulation of SCF (Jin et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Lactobacillus johnsonii BS15 improves intestinal environment against fluoride-induced memory impairment in mice—a study based on the gut–brain axis hypothesis

Xin

Zeng

Wang

et al. 2020

PeerJ

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Background Excessive fluoride can lead to chronic neurodegeneration characterized by neuron and myelin loss and memory dysfunction. The gut–brain axis hypothesis suggests that gut microbiota plays a crucial role in regulating brain function. Thus, using probiotics to adjust the gut microenvironment may be a potential therapy for mental diseases. Methods Mice in the prob group were administrated with Lactobacillus johnsonii BS15 for 28 days prior to and throughout a 70-day exposure to sodium fluoride. The drinking water of all groups (F and prob groups) except the control group were replaced by high-fluoride water (100 mg NaF/L) on day 28. Animals in each group were divided into two subsets: one underwent behavioral test, and the other was sacrificed for sampling. The mRNA expression level and protein content related to inflammatory reaction in the ileum and hippocampus were respectively detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA). The mRNA expression levels of proteins related to myelin structure, apoptosis, and memory in the hippocampus and tight junction proteins in the ileum were determined by RT-qPCR and/or immunohistochemistry. Gut permeability markers (D-lactate and diamine oxidase (DAO)) in the serum were also examined by ELISA. Results The results showed that fluoride exposure induced a lower spontaneous exploration (P < 0.05) in T-maze test, which indicated an impairment of memory. Spontaneous exploration of BS15-treated mice was significantly higher (P < 0.05) than that in F group. Fluoride reduced (P < 0.05) levels of myelin structural protein (proteolipid protein) and neurogenesis-associated proteins (brain-derived neurotrophic factor and cAMP/Ca2+ responsive element-binding protein), induced disordered inflammatory cytokines (TNF-α, IFN-γ, and IL-6; P < 0.05), increased pro-apoptotic genes (caspase-3; P < 0.05), and decreased anti-apoptotic genes (Bcl-2; P < 0.05) in the hippocampus, of which the influences were reversed by BS15. BS15 treatment exerted significant preventive effects on reversing the gut inflammation induced by excessive fluoride intake by reducing (P < 0.05) the levels of pro-inflammatory cytokines (tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ)) and remarkably increasing (P < 0.05) the level of anti-inflammatory cytokines (IL-10). Moreover, the serum DAO activity and D-lactate concentration significantly increased by fluoride were also reduced (P < 0.05) by BS15. This result indicated the profitable effect of BS15 on gut permeability. Conclusion L. johnsonii BS15 intake could benefit the neuroinflammation and demyelination in the hippocampus by improving the gut environment and ameliorating fluorine-induced memory dysfunction.

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Section: Discussionmentioning

confidence: 99%

Lactobacillus johnsonii BS15 improves intestinal environment against fluoride-induced memory impairment in mice—a study based on the gut–brain axis hypothesis

Xin

Zeng

Wang

et al. 2020

PeerJ

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“…In some cases, probiotic colonization may be optional for their effects to manifest. For instance, heat-killed L. paracasei benefited the human and animal host, in terms of neurochemical and behavioral changes (Corpuz et al, 2018;Murata et al, 2018;Wei et al, 2019). Some probiotics, such as L. reuteri, L. paracasei, L. plantarum, L. gasseri, L. kefiranofaciens, B. breve, and B. infantis, promoted the colonization of other beneficial microbes that contributed to the reduction of depressive-like symptoms in animals (Marin et al, 2017;Dhaliwal et al, 2018;Jang et al, 2019;Sun et al, 2019;Tian et al, 2019;Wei et al, 2019).…”

Section: Heterogeneity Of Gut Microbiota Compositionmentioning

confidence: 99%

“…Behavioral assessments for memory function in mice include the Morris water maze, Barnes maze and other behavioral tests (Dedic et al, 2011). Administration of probiotics including L. helveticus (Ohland et al, 2013;Luo et al, 2014;Liang et al, 2015), L. plantarum (Dhaliwal et al, 2018), and L. paracasei (Corpuz et al, 2018;Huang et al, 2018) enabled animals to perform these memory test more effectively. Attention, memory and learning behaviors in humans are assessed by cognitive tests, such as the Stroop, verbal-learning and digit-symbol tests.…”

Section: Heterogeneity Of Depressionmentioning

confidence: 99%

Antidepressive Mechanisms of Probiotics and Their Therapeutic Potential

et al. 2020

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The accumulating knowledge of the host-microbiota interplay gives rise to the microbiota-gut-brain (MGB) axis. The MGB axis depicts the interkingdom communication between the gut microbiota and the brain. This communication process involves the endocrine, immune and neurotransmitters systems. Dysfunction of these systems, along with the presence of gut dysbiosis, have been detected among clinically depressed patients. This implicates the involvement of a maladaptive MGB axis in the pathophysiology of depression. Depression refers to symptoms that characterize major depressive disorder (MDD), a mood disorder with a disease burden that rivals that of heart diseases. The use of probiotics to treat depression has gained attention in recent years, as evidenced by increasing numbers of animal and human studies that have supported the antidepressive efficacy of probiotics. Physiological changes observed in these studies allow for the elucidation of probiotics antidepressive mechanisms, which ultimately aim to restore proper functioning of the MGB axis. However, the understanding of mechanisms does not yet complete the endeavor in applying probiotics to treat MDD. Other challenges remain which include the heterogeneous nature of both the gut microbiota composition and depressive symptoms in the clinical setting. Nevertheless, probiotics offer some advantages over standard pharmaceutical antidepressants, in terms of residual symptoms, side effects and stigma involved. This review outlines antidepressive mechanisms of probiotics based on the currently available literature and discusses therapeutic potentials of probiotics for depression.

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“…The spatial learning and memory ability of mice was evaluated using the Barnes maze test as previously described [19]. The escape latency to reach the escape box and staying time in each quadrant were recorded during the probe test.…”

Section: Barnes Maze Testmentioning

confidence: 99%

Oral Administration of Okara Soybean By-Product Attenuates Cognitive Impairment in a Mouse Model of Accelerated Aging

et al. 2019

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The microbiota–gut–brain axis has attracted increasing attention in the last decade. Here, we investigated whether okara, a soybean by-product rich in dietary fiber, can attenuate cognitive impairment in senescence-accelerated mouse prone 8 (SAMP8) mice by altering gut microbial composition. Mice were fed either a standard diet, or a diet containing okara (7.5% or 15%, w/w) for 26 weeks. In the memory test, the 7.5% okara-fed mice showed a longer step-through latency and the 15% okara-fed mice had a short escape latency compared with control mice. The 15% okara-fed mice displayed decreased body weight, increased fecal weight, and altered cecal microbiota composition compared with the control group; however, there was no significant difference in the serum lactic acid and butyric acid levels among these mice groups. The 7.5% okara-fed mice had significantly higher NeuN intensity in the hippocampus compared with control mice. Furthermore, a decrease in inflammatory cytokine TNF-α and an increase in brain-derived neurotrophic factor (BDNF) was observed in the 7.5% okara-fed group. The expression of synthesizing enzyme of acetylcholine was increased by the okara diets, and the acetylcholine level in the brain was higher in the 7.5% okara-fed group than in the control. These suggest that oral administration of okara could delay cognitive decline without drastically changing gut microbiota.

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Long-Term Diet Supplementation with Lactobacillus paracasei K71 Prevents Age-Related Cognitive Decline in Senescence-Accelerated Mouse Prone 8

Cited by 52 publications

References 33 publications

Lactobacillus johnsonii BS15 improves intestinal environment against fluoride-induced memory impairment in mice—a study based on the gut–brain axis hypothesis

Lactobacillus johnsonii BS15 improves intestinal environment against fluoride-induced memory impairment in mice—a study based on the gut–brain axis hypothesis

Antidepressive Mechanisms of Probiotics and Their Therapeutic Potential

Oral Administration of Okara Soybean By-Product Attenuates Cognitive Impairment in a Mouse Model of Accelerated Aging

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