المؤلفون: Choi, Hyo-Sun, Kim, Joonki^{Aff2, Aff4}, Lee, Sang-Bin, Zhang, Lijun^{Aff2, Aff3}, Kwon, Dowan, Tran, Huynh Nguyen Khanh, Zhang, Siqi^{Aff2, Aff4}, Huang, Tianqi^{Aff1, Aff3}, Yu, Jae Sik, Lee, Gakyung, Yang, Hyun Ok^{Aff1, Aff2, Aff3, IDs12035024042420_cor11}

المصدر: Molecular Neurobiology. :1-16

المؤلفون: Tientcheu, Jean Philippe Djientcheu, Ngueguim, Florence Tsofack^{Aff1, IDs11011023012917_cor2}, Gounoue, Racéline Kamkumo, Mbock, Michel Arnaud, Ngapout, Rodrigue, Kandeda, Antoine Kavaye, Dimo, Théophile

المصدر: Metabolic Brain Disease. 38(8):2773-2796

المؤلفون: Xue Wang, Yuhan Wu, Yingrui Tian, Hui Hu, Yun Zhao, Binghua Xue, Zhaowei Sun, Aijun Wei, Fang Xie, Ling-Jia Qian

المصدر: Cell & Bioscience, Vol 14, Iss 1, Pp 1-21 (2024)

مصطلحات موضوعية: Chronic stress, Microglia, Proinflammatory activation, GLUT1, Spatial memory dysfunction, Biotechnology, TP248.13-248.65, Biology (General), QH301-705.5, Biochemistry, QD415-436

الوصف: Abstract Background Stress is a recognized risk factor for cognitive decline, which triggers neuroinflammation involving microglial activation. However, the specific mechanism for microglial activation under stress and affects learning and memory remains unclear. Methods The chronic stress mouse model was utilized to explore the relationship between microglial activation and spatial memory impairment. The effect of hippocampal hyperglycemia on microglial activation was evaluated through hippocampal glucose-infusion and the incubation of BV2 cells with high glucose. The gain-and loss-of-function experiments were conducted to investigate the role of GLUT1 in microglial proinflammatory activation. An adeno-associated virus (AAV) was employed to specifically knockdown of GLUT1 in hippocampal microglia to assess its impact on stressed-mice. Results Herein, we found that chronic stress induced remarkable hippocampal microglial proinflammatory activation and neuroinflammation, which were involved in the development of stress-related spatial learning and memory impairment. Mechanistically, elevated hippocampal glucose level post-stress was revealed to be a key regulator of proinflammatory microglial activation via specifically increasing the expression of microglial GLUT1. GLUT1 overexpression promoted microglial proinflammatory phenotype while inhibiting GLUT1 function mitigated this effect under high glucose. Furthermore, specific downregulation of hippocampal microglial GLUT1 in stressed-mice relieved microglial proinflammatory activation, neuroinflammation, and spatial learning and memory injury. Finally, the NF-κB signaling pathway was demonstrated to be involved in the regulatory effect of GLUT1 on microglia. Conclusions We demonstrate that elevated glucose and GLUT1 expression induce microglia proinflammatory activation, contributing to stress-associated spatial memory dysfunction. These findings highlight significant interplay between metabolism and inflammation, presenting a possible therapeutic target for stress-related cognitive disorders.

وصف الملف: electronic resource

Relation: https://doaj.org/toc/2045-3701

URL الوصول: https://doaj.org/article/16f82017a1a1420697bd7bd219f07fbc

المؤلفون: Fatemeh Mohammadinia, Saeed Esmaeili‐Mahani, Mehdi Abbasnejad, Manijeh Dogani, Ali Mohammad Poorrahimi

المصدر: Brain and Behavior, Vol 14, Iss 5, Pp n/a-n/a (2024)

مصطلحات موضوعية: CA1, capsaicin, learning and memory dysfunction, methyl jasmonate, orofacial pain, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571

الوصف: Abstract Objective Orofacial pain with high prevalence is one of the substantial human health issues. The importance of this matter became more apparent when it was revealed that orofacial pain, directly and indirectly, affects cognition performances. Currently, researchers have focused on investigating pharmaceutics to alleviate pain and ameliorate its subsequent cognitive impairments. Design In this study, the rats were first treated with the central administration of methyl jasmonate (MeJA), which is an antioxidant and anti‐inflammatory bio‐compound. After 20 min, orofacial pain was induced in the rats by the injection of capsaicin in their dental pulp. Subsequently, the animals’ pain behaviors were analyzed, and the effects of pain and MeJA treatments on rats learning and memory were evaluated/compared using the Morris water maze (MWM) test. In addition, the expression of tumor necrosis factor‐α (TNF‐α), IL‐1β, BDNF, and COX‐2 genes in the rats’ hippocampus was evaluated using real‐time polymerase chain reaction. Results Experiencing orofacial pain resulted in a significant decline in the rats learning and memory. However, the central administration of 20 μg/rat of MeJA effectively mitigated these impairments. In the MWM, the performance of the MeJA‐treated rats showed a two‐ to threefold improvement compared to the nontreated ones. Moreover, in the hippocampus of pain‐induced rats, the expression of pro‐inflammatory factors TNF‐α, IL‐1β, and COX‐2 significantly increased, whereas the BDNF expression decreased. In contrast, MeJA downregulated the pro‐inflammatory factors and upregulated the BDNF by more than 50%. Conclusions These findings highlight the notable antinociceptive potential of MeJA and its ability to inhibit pain‐induced learning and memory dysfunction through its anti‐inflammatory effect.

وصف الملف: electronic resource

Relation: https://doaj.org/toc/2162-3279

URL الوصول: https://doaj.org/article/b55d3c861e2c4ba4984e153e06feade9

المؤلفون: Islamie, Ridho, Myint, Su Lwin Lwin, Rojanaratha, Tissana, Ritthidej, Garnpimol^{Aff2, Aff3}, Wanakhachornkrai, Oraphan, Wattanathamsan, Onsurang, Rodsiri, Ratchanee^{Aff1, Aff5, IDs12906023041252_cor7}

المصدر: BMC Complementary Medicine and Therapies. 23(1)

المؤلفون: Ridho Islamie, Su Lwin Lwin Myint, Tissana Rojanaratha, Garnpimol Ritthidej, Oraphan Wanakhachornkrai, Onsurang Wattanathamsan, Ratchanee Rodsiri

المصدر: BMC Complementary Medicine and Therapies, Vol 23, Iss 1, Pp 1-18 (2023)

مصطلحات موضوعية: Asiatic acid, SLNs, Nose-to-brain, Amyloid beta, Memory dysfunction, Mice, Other systems of medicine, RZ201-999

الوصف: Abstract Background Amyloid-β1-42 (Aβ1-42) plays an essential role in the development of the early stage of Alzheimer’s disease (AD). Asiatic acid (AA), an active compound in Centella asiatica L, exhibit neuroprotective properties in previous studies. Due to its low bioavailability, the nose-to-brain delivery technique was used to enhance AA penetration in the brain. In this study, AA was also loaded in solid lipid nanoparticles (SLNs) as a strategy to increase its absorption in the nasal cavity. Methods Memory impairment was induced via direct intracerebroventricular injection of Aβ1-42 oligomer into mouse brain. The neuroprotective effect and potential underlying mechanisms were investigated using several memory behavioral examinations and molecular techniques. Results The intranasal administration of AA in SLNs attenuated learning and memory impairment induced by Aβ1-42 in Morris water maze and novel object recognition tests. AA significantly inhibited tau hyperphosphorylation of pTau-S396 and pTau-T231 and prevented astrocyte reactivity and microglial activation in the hippocampus of Aβ1-42-treated mice. It is also decreased the high levels of IL-1β, TNF-α, and malondialdehyde (MDA) in mouse brain. Conclusions These results suggested that nose-to-brain delivery of AA in SLNs could be a promising strategy to treat the early stage of AD.

وصف الملف: electronic resource

Relation: https://doaj.org/toc/2662-7671

URL الوصول: https://doaj.org/article/3a607e70f06a4c30b0649f56c85570f1

المؤلفون: Huo, Kang, Wei, Meng, Zhang, Meng, Wang, Zhanqiang, Pan, Peipei, Shaligram, Sonali S, Huang, Jinhao, Do Prado, Leandro B, Wong, Julia, Su, Hua

المصدر: Cerebrovascular and Brain Metabolism Reviews. 41(9)

مصطلحات موضوعية: Biomedical and Clinical Sciences, Neurosciences, Clinical Sciences, Stroke, Brain Disorders, Aging, Neurological, Animals, Disease Models, Animal, Female, Fractures, Bone, Humans, Inflammation, Male, Memory, Long-Term, Mice, Post-stroke memory dysfunction, neuroinflammation, alpha-7 nicotinic acetylcholine receptor, bone fracture, ischemic stroke, Cardiorespiratory Medicine and Haematology, Neurology & Neurosurgery, Clinical sciences

الوصف: Tibia fracture (BF) enhances stroke injury and post-stroke memory dysfunction in mouse. Reduction of neuroinflammation by activation of α-7 nicotinic acetylcholine receptor (α-7 nAchR) reduced acute neuronal injury and sensorimotor dysfunction in mice with BF 1-day after stroke. We hypothesize that reduction of neuroinflammation by activation of α-7 nAchR improves long-term memory function of mice with BF 6-h before stroke. The mice were randomly assigned to saline, PHA-568487 (α-7 nAchR agonist) and methyllycaconitine (antagonist) treatment groups. The sensorimotor function was tested by adhesive removal and corner tests at 3 days, the memory function was tested by Y-maze test weekly for 8 weeks and novel objective recognition test at 8 weeks post-injuries. We found PHA-568487 treatment reduced, methyllycaconitine increased the number of CD68+ cells in the peri-infarct and hippocampal regions, neuronal injury in the infarct region, sensorimotor and long-term memory dysfunctions. PHA-568487 treatment also reduced, while methyllycaconitine treatment increased atrophy of hippocampal granule cell layer and white matter damage in the striatum. In addition, PHA-568487 treatment increased neuron proliferation in granule cell layer. Our data indicated that reduction of neuroinflammation through activation of α-7 nAchR decreased neuronal damage, sensorimotor and long-term memory dysfunction of mice with BF shortly before stroke.

وصف الملف: application/pdf

URL الوصول: https://escholarship.org/uc/item/0rc5r4q0

المؤلفون: Wang, Xue, Wu, Yuhan, Tian, Yingrui^{Aff1, Aff2}, Hu, Hui, Zhao, Yun, Xue, Binghua, Sun, Zhaowei, Wei, Aijun, Xie, Fang^{Aff1, IDs13578024012291_cor9}, Qian, Ling-Jia^{Aff1, IDs13578024012291_cor10}

المصدر: Cell & Bioscience. 14(1)

المؤلفون: El-Sayed, Norhan S., Elatrebi, Soha, Said, Rasha, Ibrahim, Heba F., Omar, Eman M.^{Aff1, IDs1101102201035z_cor5}

المصدر: Metabolic Brain Disease. 37(7):2375-2388

المؤلفون: Xufei Zhang, Xianhao Jia, Shengnan Wang, Jinge Xin, Ning Sun, Yanyan Wang, Xingting Zhang, Zhiqiang Wan, Jing Fan, Hao Li, Yang Bai, Xueqin Ni, Yongmei Huang, Hesong Wang, Hailin Ma

المصدر: Ecotoxicology and Environmental Safety, Vol 259, Iss , Pp 115035- (2023)

مصطلحات موضوعية: High altitude environment, Microbiome-gut-brain axis, Spatial memory dysfunction, Antibiotics, Probiotics, Environmental pollution, TD172-193.5, Environmental sciences, GE1-350

الوصف: Approximately 400 million people work and live in high-altitude areas and suffer from memory dysfunction worldwide. Until now, the role of the intestinal flora in plateau-induced brain damage has rarely been reported. To address this, we investigated the effect of intestinal flora on spatial memory impairment induced by high altitudes based on the microbiome–gut–brain axis theory. C57BL/6 mice were divided into three groups: control, high-altitude (HA), and high-altitude antibiotic treatment (HAA) group. The HA and HAA groups were exposed to a low-pressure oxygen chamber that simulated an altitude of 4000 m above sea level (m. a. s.l.) for 14 days, with the air pressure in the chamber set at 60–65 kPa. The results showed that spatial memory dysfunction induced by the high-altitude environment was aggravated by antibiotic treatment, manifesting as lowered escape latency and hippocampal memory-related proteins (BDNF and PSD-95). 16 S rRNA sequencing showed a remarkable separation of the ileal microbiota among the three groups. Antibiotic treatment exacerbated the reduced richness and diversity of the ileal microbiota in mice in the HA group. Lactobacillaceae were the main target bacteria and were significantly reduced in the HA group, which was exacerbated by antibiotic treatment. Meanwhile, reduced intestinal permeability and ileal immune function in mice exposed high-altitude environment was also aggravated by antibiotic treatment, as indicated by the lowered tight junction proteins and IL-1β and IFN-γ levels. Furthermore, indicator species analysis and Netshift co-analysis revealed that Lactobacillaceae (ASV11) and Corynebacteriaceae (ASV78, ASV25, and ASV47) play important roles in high-altitude exposure-induced memory dysfunction. Interestingly, ASV78 was negatively correlated with IL-1β and IFN-γ levels, indicating that ASV78 may be induced by reduced ileal immune function, which mediates high-altitude environment exposure-induced memory dysfunction. This study provides evidence that the intestinal flora is effective in preventing brain dysfunction caused by exposure to high-altitude environments, suggesting a relationship between the microbiome–gut–brain axis and altitude exposure.

وصف الملف: electronic resource

Relation: http://www.sciencedirect.com/science/article/pii/S0147651323005390; https://doaj.org/toc/0147-6513

URL الوصول: https://doaj.org/article/60f58eefb2944880bc6d2b9933c6adfe