scholarly journals Powdered Green Tea (Matcha) Attenuates the Cognitive Dysfunction via the Regulation of Systemic Inflammation in Chronic PM2.5-Exposed BALB/c Mice

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1932
Author(s):  
Jong Min Kim ◽  
Jin Yong Kang ◽  
Seon Kyeong Park ◽  
Jong Hyun Moon ◽  
Min Ji Kim ◽  
...  

This study was conducted to evaluate the anti-amnesic effect of the aqueous extract of powdered green tea (matcha) (EM) in particulate matter (PM)2.5-induced systemic inflammation in BALB/c mice. EM ameliorated spatial learning and memory function, short-term memory function, and long-term learning and memory function in PM2.5-induced mice. EM protected against antioxidant deficit in pulmonary, dermal, and cerebral tissues. In addition, EM improved the cholinergic system through the regulation of acetylcholine (ACh) levels and acetylcholinesterase (AChE) activity in brain tissue, and it protected mitochondrial dysfunction by regulating the production of reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and ATP contents in brain tissue. EM attenuated systemic inflammation and apoptotic signaling in pulmonary, dermal, olfactory bulb, and hippocampal tissues. Moreover, EM suppressed neuronal cytotoxicity and cholinergic dysfunction in hippocampal tissue. This study suggests that EM might be a potential substance to improve PM2.5-induced cognitive dysfunction via the regulation of systemic inflammation.

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Katrina Jew ◽  
Denise Herr ◽  
Candace Wong ◽  
Andrea Kennell ◽  
Keith Morris-Schaffer ◽  
...  

Abstract Background A growing body of epidemiological literature indicates that particulate matter (PM) air pollution exposure is associated with elevated Alzheimer’s disease (AD) risk and may exacerbate AD-related cognitive decline. Of concern is exposure to the ultrafine PM (UFP) fraction (≤100 nm), which deposits efficiently throughout the respiratory tract, has higher rates of translocation to secondary organs, like brain, and may induce inflammatory changes. We, therefore, hypothesize that exposure to UFPs will exacerbate cognitive deficits in a mouse model of AD. The present study assessed alterations in learning and memory behaviors in aged (12.5 months) male 3xTgAD and non-transgenic mice following a 2-week exposure (4-h/day, 4 days/week) to concentrated ambient UFPs using the Harvard ultrafine concentrated ambient particle system (HUCAPS) or filtered air. Beginning one month following exposure, locomotor activity, spatial learning and memory, short-term recognition memory, appetitive motivation, and olfactory discrimination were assessed. Results No effects on locomotor activity were found following HUCAPS exposure (number concentration, 1 × 104–4.7 × 105 particles/cm3; mass concentration, 29–132 μg/m3). HUCAPS-exposed mice, independent of AD background, showed a significantly decreased spatial learning, mediated through reference memory deficits, as well as short-term memory deficits in novel object recognition testing. AD mice displayed diminished spatial working memory, potentially a result of olfactory deficits, and short-term memory. AD background modulated HUCAPS-induced changes on appetitive motivation and olfactory discrimination, specifically enhancing olfactory discrimination in NTg mice. Modeling variation in appetitive motivation as a covariate in spatial learning and memory, however, did not support the conclusion that differences in motivation significantly underlie changes in spatial learning and memory. Conclusions A short-term inhalation exposure of aged mice to ambient UFPs at human-relevant concentrations resulted in protracted (testing spanning 1–6.5 months post-exposure) adverse effects on multiple memory domains (reference and short-term memory) independent of AD background. Impairments in learning and memory were present when accounting for potential covariates like motivational changes and locomotor activity. These results highlight the need for further research into the potential mechanisms underlying the cognitive effects of UFP exposure in adulthood.


2020 ◽  
Vol 77 (2) ◽  
pp. 629-640
Author(s):  
Li Hu ◽  
Shaoping Zhu ◽  
Xiaoping Peng ◽  
Kanglan Li ◽  
Wanjuan Peng ◽  
...  

Background: Excessive salt intake is considered as an important risk factor for cognitive impairment, which might be the consequence of imbalanced intestinal homeostasis. Objective: To investigate the effects of dietary salt on the gut microbiota and cognitive performance and the underlying mechanisms. Methods: Adult female C57BL/6 mice were maintained on either normal chow (control group, CON) or sodium-rich chow containing 8% NaCl (high-salt diet, HSD) for 8 weeks. Spatial learning and memory ability, short-chain fatty acids (SCFAs) concentrations, gut bacterial flora composition, blood-brain barrier permeability, and proinflammatory cytokine levels and apoptosis in the brain were evaluated. Results: The mice fed a HSD for 8 weeks displayed impaired learning and memory abilities. HSD significantly reduced the proportions of Bacteroidetes (S24-7 and Alloprevotella) and Proteobacteria and increased that of Firmicutes (Lachnospiraceae and Ruminococcaceae). SCFA concentrations decreased in the absolute concentrations of acetate, propionate, and butyrate in the fecal samples from the HSD-fed mice. The HSD induced both BBB dysfunction and microglial activation in the mouse brain, and increased the IL-1β, IL-6, and TNF-α expression levels in the cortex. More importantly, the degree of apoptosis was higher in the cortex and hippocampus region of mice fed the HSD, and this effect was accompanied by significantly higher expression of cleaved caspase-3, caspase-3, and caspase-1. Conclusion: The HSD directly causes cognitive dysfunction in mice by eliciting an inflammatory environment and triggering apoptosis in the brain, and these effects are accompanied by gut dysbiosis, particularly reduced SCFA production.


2020 ◽  
Vol 30 (9) ◽  
pp. 4964-4978 ◽  
Author(s):  
Ivana Kiroski ◽  
Yulan Jiang ◽  
Cezar Gavrilovici ◽  
Fan Gao ◽  
Sukyoung Lee ◽  
...  

Abstract The glycoprotein Reelin maintains neuronal positioning and regulates neuronal plasticity in the adult brain. Reelin deficiency has been associated with neurological diseases. We recently showed that Reelin is depleted in mice with a targeted disruption of the Ndel1 gene in forebrain postnatal excitatory neurons (Ndel1 conditional knockout (CKO)). Ndel1 CKO mice exhibit fragmented microtubules in CA1 pyramidal neurons, profound deterioration of the CA1 hippocampus and a shortened lifespan (~10 weeks). Here we report that Ndel1 CKO mice (of both sexes) experience spatial learning and memory deficits that are associated with deregulation of neuronal cell adhesion, plasticity and neurotransmission genes, as assessed by genome-wide transcriptome analysis of the hippocampus. Importantly, a single injection of Reelin protein in the hippocampus of Ndel1 CKO mice improves spatial learning and memory function and this is correlated with reduced intrinsic hyperexcitability of CA1 pyramidal neurons, and normalized gene deregulation in the hippocampus. Strikingly, when treated with Reelin, Ndel1 CKO animals that die from an epileptic phenotype, live twice as long as nontreated, or vehicle-treated CKO animals. Thus, Reelin confers striking beneficial effects in the CA1 hippocampus, and at both behavioral and organismal levels.


2008 ◽  
Vol 29 (6) ◽  
pp. 940-947 ◽  
Author(s):  
Tin-Tin Win-Shwe ◽  
Shoji Yamamoto ◽  
Yuji Fujitani ◽  
Seishiro Hirano ◽  
Hidekazu Fujimaki

2018 ◽  
Vol 1 (4) ◽  
Author(s):  
Weidong Sun ◽  
Jian Zhou

Objective Proper participation in physical exercise can not only benefit people physically, but also promote people's psychological benefits. However, people are often only aware of the benefits of physical exercise, such as physical fitness, body shape and function, and ignore the psychological benefits caused by physical exercise. In recent years, more and more people pay attention to the positive psychological benefits of physical exercise on cognition. As the hope of the future of the country, the problem of physical health is widely concerned. To study the effect of physical exercise on children's cognitive function, and to analyze the possible biological mechanism of physical exercise affecting cognitive ability, and to provide a reference for promoting the good development of children's physique. Methods  Through the retrieval of Chinese knowledge network, Wanfang Data knowledge service platform, VVP cube knowledge discovery system, 100 chain database collection sports related research literature, collating literature information, in-depth integration of literature, analysis of the impact and mechanism of physical exercise on children's cognition. Results  (1) Physical exercise can improve the function of the brain, improve the efficiency of the brain, and enhance memory. Animal experiments have shown that physical exercise can enhance short-term memory by improving hippocampal function in rats. (2) Regular physical exercise can improve children's memory and executive function, and promote their cognitive function and academic performance. (3) The effect of physical exercise on specific cognitive function is in turn motor function, motor skills, academic performance, reasoning, reaction time and executive function. Physical exercise promotes cognitive performance by improving the goal of the brain pointing to the maintenance of processing, but physical exercise does not improve or slow down processing inhibition, and physical exercise is not related to processing inhibition. 30 minutes of acute physical exercise plays a significant role in maintaining children's attention. Acute high intensity physical exercise can improve selective attention and short-term memory tasks. In the experiment of the effect of one-off acute physical exercise on cognitive function, moderate intensity of heart rate variables and increased cognitive performance were related. For children with attention deficit hyperactivity disorder, physical exercise can improve their performance of executive function. (4) Physical exercise may affect the possible biological mechanisms of cognitive function: Firstly, exercise can improve the synthesis and secretion of neurotransmitters such as acetylcholine and dopamine, activate conduction pathways, improve synaptic transmission efficiency, and promote the development of learning and memory function. Secondly, exercise can increase brain derived neurotrophic factor (BDN F), release of nerve growth factors such as insulin-like growth factor --1 (IGF--1) and so on, thus promoting the development of learning and memory function. Again, physical exercise may also improve learning and memory performance by affecting the release of glucocorticoids. Then, physical exercise can enhance the gene expression in the brain area related to learning and memory. Finally, physical exercise may maintain and improve cognitive ability by improving the antioxidant capacity of brain tissue. Conclusions Physical exercise can promote the improvement of children's cognitive ability. The basic cognitive ability of children can be developed through physical exercise. The mechanism of the exercise can be explained by the changes of the brain nerve mechanism, such as increasing the brain capacity and increasing the flow velocity of the brain. The specific biological mechanism still needs to be studied.


2021 ◽  
pp. 1-11
Author(s):  
Yanhu Ge ◽  
Duomao Lin ◽  
Boqun Cui ◽  
Liang Zhang ◽  
Shurong Li ◽  
...  

<b><i>Introduction:</i></b> Isoflurane (ISO) may cause neuronal apoptosis and synaptic disorder during development, and damage long-term learning and memory function. This observation aimed to study the function of H19 in vitro and in vivo tests and the further mechanism was identified. <b><i>Methods:</i></b> ISO cell models and rat models were established and reactive oxygen species (ROS) identified. The viability and apoptosis of HT22 cells were detected by the MTT and flow cytometer. Morris water maze test was conducted to analyze the neurotoxicity of ISO on spatial learning and memory ability. Quantitative PCR was the method to verify the expression of H19. The concentration of inflammatory indicators was identified by enzyme-linked immunosorbent assay. <b><i>Results:</i></b> 1.5% and 2% ISO led to the neurotoxicity of HT22 cells and increased expression of H19. Silenced H19 meliorated these adverse impacts of ISO. Interference of H19 exerted neuroprotective roles by repressing modified neurological severity score, inhibiting escape latency, elevating distance and time of target area, and controlling ROS and inflammation. MiR-17-5p might be a promising competing endogenous RNA of H19. The expression of miR-17-5p was reduced in the ISO group and reversed by the absence of H19. <b><i>Conclusion:</i></b> Our results of in vitro and in vivo assay indicated that the absence of HT22 is a neuroprotective regulator of cognition and inflammation by accumulating miR-17-5p.


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