INTERNATIONAL JOURNAL OF TECHNOLOGY AND DESIGN EDUCATION
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2024
·Vol. 34
·期 5
·1687-1704
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IF 2
Cai Lu
Based on Folk theory, Media Equation, and AI literacy research, the study constructed an interview outline and selected 72 students in 4th and 5th grade in three primary schools located in the Minhang and Putuo districts of Shanghai (two in the Minhang district and one in the Putuo district) as the study participants for focus group interviews. The study found that the availability of voice interaction is an essential basis for children to judge the level of intelligence of a machine; additionally, chatting is also the starting point for young children to build a close relationship with AI. Although AI cannot replace their friends, it can become a friend to them. While children expect the future of AI to be beyond the current level of intelligence and emotion and to enable the full use of machines in multiple scenarios and various fields, they are also concerned about issues such as privacy breaches that devices may cause in the future and believe that technology should not develop outside of human control.
研究领域:
教育心理学
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人机交互
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儿童发展研究
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DOI
高影响因子
JOURNAL OF NEUROIMMUNOLOGY
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2025
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IF 2.5
Weiwei Ji,Zengyu Zhang,Tingyu Jin,Danyang Meng,Xuyou Zhou,Jin Hu,Yong Wang
Background Chronic cerebral hypoperfusion (CCH) is a significant contributor to vascular cognitive impairment (VCI), often linked to cortical and hippocampal damage. This study investigates the therapeutic potential of salidroside (SLDS) in mitigating CCH-induced brain injury by modulating microglial activation and inflammatory responses. Methods We established a CCH model in mice using the 0.16/0.18 mm bilateral common carotid artery stenosis (BCAS) procedure. We assessed cerebral blood flow (CBF) via laser speckle contrast imaging, while neuropathology was evaluated through Nissl staining and immunofluorescence (IF) experiments. Cognitive deficits were measured using the Morris water maze test. Neuronal apoptosis and neuroinflammation were examined through IF, ELISA, and qRT-PCR. Results BCAS-induced hypoperfusion resulted in a marked reduction in CBF, increased neuronal apoptosis, and significant cognitive deficits. SLDS treatment effectively countered these effects by shifting microglial polarization from a pro-inflammatory M1 phenotype to an anti-inflammatory M2 phenotype, reducing pro-inflammatory cytokine levels, and enhancing neuronal survival. Conclusion SLDS demonstrates strong neuroprotective potential against CCH-induced brain injury by reducing inflammation and preventing neuronal apoptosis. These findings highlight the promise of SLDS as a therapeutic agent for chronic cerebrovascular disorders, warranting further investigation into its molecular mechanisms and clinical applicability.
研究领域:
神经科学
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药理学
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分子生物学
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DOI
PubMed
高影响因子
ACTA PHARMACOLOGICA SINICA
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2025
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IF 8.4
Feng Yue-yao,Hao Jing-ran,Zhang Yu-jie,Qiu Tong-tong,Zhang Meng-lin,Qiao Wei,Wu Jin-jin,Qiu Ping,Xu Chao-fan,Zhang Yin-liang,Du Chun-yuan,Pan Zhe,Chang Yong-sheng
The deposition of β-amyloid (Aβ) in the brain is a crucial factor in the pathogenesis of Alzheimer’s disease (AD). Insulin-degrading enzyme (IDE) plays a critical role in the balance between Aβ production and degradation. However, the regulatory mechanisms of IDE are not yet fully understood. Therefore, uncovering additional IDE regulatory mechanisms will help elucidate the pathogenesis of AD and identify key therapeutic targets for this disease. This study revealed that global Krüppel-like factor 9-mutant (Klf9 −/− ) mice exhibited impaired cognitive function. Additionally, we found that Klf9 expression in hippocampal tissue was reduced in APPswe/PS1dE9 (APP/PS1) mice. This study also showed that Klf9 stimulates IDE expression and promotes the Aβ degradation process by directly binding to IDE and activating its transcription. Silencing IDE blocked the Klf9-induced Aβ degradation process. We stereotactically injected an adeno-associated virus to selectively overexpress IDE (AAV-IDE) in the hippocampal neurons of Klf9 −/− mice and found that the overexpression of IDE in hippocampal neurons ameliorated cognitive deficits and reduced the Aβ content in Klf9 −/− mice. Additionally, we also stereotactically injected AAV-Klf9 into the hippocampal neurons of APP/PS1 mice and found that overexpression of Klf9 in hippocampal neurons ameliorated cognitive deficits and reduced Aβ levels in APP/PS1 mice. These findings suggest that downregulation of Klf9 may be a key factor in AD progression, as it reduces Aβ clearance by decreasing IDE expression. Overexpression or activation of Klf9 may be a potential strategy for preventing the pathogenesis of AD.
研究领域:
神经生物学
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分子生物学
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医学
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
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2023
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IF 5.6
Jun Liu,Tao Gao,Bin Zhou,Xiaoxiao Xu,Xiaojie Zhai,Qinghuan Yao,Xiaowei Chen,Lin Liu,Wei Cui,Xiang Wu
Postoperative cognitive dysfunction (POCD) is a decline in cognitive function affecting the mental health of aged patients after surgery. The pathological mechanisms underlying POCD have not yet been clarified. The overexpression of the P2X4 receptor in the central nervous system (CNS) was reported to be associated with the onset of POCD. Fast green FCF (FGF), a widely used food dye, could decrease the expression of the P2X4 receptor in the CNS. This study aimed to explore whether FGF could prevent POCD via the down-regulation of CNS P2X4 receptor. Exploratory laparotomy under the anesthesia of fentanyl and droperidol was carried to establish an animal model of POCD in 10–12-months-olds mice. FGF significantly attenuated cognitive impairments and down-regulated the expression of the P2X4 receptor induced by surgery in mice. Moreover, the blockade of CNS P2X4 receptor by intrahippocampal injection of 5-BDBD induced cognitive-enhancing effects on POCD mice. In addition, the effects of FGF were abolished by ivermectin, which is a positive allosteric modulator of the P2X4 receptor. FGF also inhibited M1 polarization of microglia cells, decreased the phosphorylation of nuclear factor-κB (NF-κB), and reduced the production of pro-inflammatory cytokines. These results suggested that FGF produced anti-POCD cognitive-enhancing effects via down-regulation of the P2X4 receptor-associated neuroinflammation, providing a support that FGF might be a potential treatment for POCD.
研究领域:
神经科学
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药理学
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外科手术
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分子生物学
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DOI
PubMed
高影响因子
ENVIRONMENT INTERNATIONAL
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2024
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IF 10.3
Yunting Li,Anfei Liu,Kaiju Chen,Lifan Li,Xiaoshun Zhang,Fei Zou,Xingmei Zhang,Xiaojing Meng
Lead is an environmentally widespread neurotoxic pollutant. Although the neurotoxicity of lead has been found to be closely associated with metabolic disorders, the effects of short-chain fatty acids on the neurotoxicity of lead and its mechanisms have not yet been explored. In this study, the results of open field tests and Morris water maze tests demonstrated that chronic lead exposure caused learning and memory deficits and anxiety-like symptoms in mice. The serum butyric acid content of lead-treated mice decreased in a dose-dependent manner, and oral administration of butyrate significantly improved cognitive memory impairment and anxiety symptoms in lead-exposed mice. Moreover, butyrate alleviated neuroinflammation caused by lead exposure by inhibiting the STAT3 signaling in microglia. Butyrate also promoted the expression of acetyl-CoA synthetase ACSS2 in hippocampal neurons, thereby increasing the content of acetyl-CoA and restoring the expression of both histone H3K9ac and the downstream BDNF. We also found that the median butyric acid concentration in high-lead exposure humans was remarkably lower than that in the low-lead exposure humans (45.16 μg/L vs. 60.92 μg/L, P < 0.01), and that butyric acid significantly mediated the relationship of lead exposure with the Montreal cognitive assessment scores, with a contribution rate of 27.57 %. In conclusion, our results suggest that butyrate supplementation is a possible therapeutic strategy for lead-induced neurotoxicity.
研究领域:
神经科学
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毒理学
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药理学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
Autophagy
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2024
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IF 14.6
Kateřina Veverová,Jan Laczó,Alžběta Katonová,Hana Horáková,Veronika Matušková,Francesco Angelucci,Martina Laczó,Zuzana Nedelská,Jakub Hort,He-Ling Wang,Jianying Zhang,Liu Shi,Evandro Fei Fang,Martin Vyhnálek
Defective mitophagy is consistently found in postmortem brain and iPSC-derived neurons from Alzheimer disease (AD) patients. However, there is a lack of extensive examination of mitophagy status in serum or cerebrospinal fluid (CSF), and the clinical potential of mitophagy biomarkers has not been tested. We quantified biomarkers of mitophagy/autophagy and lysosomal degradation (PINK1, BNIP3L and TFEB) in CSF and serum from 246 individuals, covering mild cognitive impairment due to AD (MCI-AD, n = 100), dementia due to AD (AD-dementia, n = 100), and cognitively unimpaired individuals (CU, n = 46), recruited from the Czech Brain Aging Study. Cognitive function and brain atrophy were also assessed. Our data show that serum and CSF PINK1 and serum BNIP3L were higher, and serum TFEB was lower in individuals with AD than in corresponding CU individuals. Additionally, the magnitude of mitophagy impairment correlated with the severity of clinical indicators in AD patients. Specifically, levels of PINK1 positively correlated with phosphorylated (p)-MAPT/tau (181), total (t)-MAPT/tau, NEFL (neurofilament light chain), and NRGN (neurogranin) levels in CSF and negatively with memory, executive function, and language domain. Serum TFEB levels negatively correlated with NEFL and positively with executive function and language. This study reveals mitophagy impairment reflected in biofluid biomarkers of individuals with AD and associated with more advanced AD pathology.Abbreviation: Aβ: amyloid beta; AD: Alzheimer disease; AVs: autophagic vacuoles; BNIP3L: BCL2 interacting protein 3 like; CU: cognitively unimpaired; CSF: cerebrospinal fluid; LAMP1: lysosomal-associated membrane protein 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MCI: mild cognitive impairment; NRGN: neurogranin; NEFL: neurofilament light chain; p-MAPT/tau: phosphorylated microtubule associated protein tau; PINK1: PTEN induced kinase 1; t-MAPT/tau: total microtubule associated protein tau; TFEB: transcription factor EB; TMT: Trail Making Test.
研究领域:
神经病学
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神经退行性疾病
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生物标志物研究
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临床神经科学
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DOI
高影响因子
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
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2024
·Vol. 79
·期 3
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IF 4.3
Wang He-Ling,Fang Evandro F
We are now living in an aging society with increasingly older population, many of whom are suffering with or are at a high risk of developing dementia (1,2). Alzheimer’s disease (AD) is the world’s most common type of dementia, affecting about 50 million individuals worldwide currently, with that number set to rise to 82 million by 2023. There is a huge challenge in developing an anti-AD drug, and an enormous amount of effort has been devoted to this branch of research. It is encouraging that the 2 recently described anti-Aβ antibodies, lecanemab and donanemab, show clear benefits in slowing cognitive decline in patients with early-stage disease; however, rare but severe side effects (such as brain bleeding and swelling) still occur (10.1126/science.adj8110), indicating that there is likely a longway to go in developing a cure for AD (3,4).Although the hunt is on to develop an anti-AD drug to stop disease progression, it is also important and necessary to focus on prevention. It has been reported that lifestyle patterns and environmental toxins (natural and anthropogenic) increase the risk of dementia, with some estimates noting up to a 30% increase in AD risk. These factors are modifiable and reducing such risks could prevent or slow down the onset of dementia (5,6). Environmental toxins cover a broad spectrum of chemicals, including pesticides (organochlorine and organophosphate insecticides), toxic metals (such as aluminum), air pollutants, and especially industrial chemicals (6). Although we are exposed to trace amount of these contaminants during our daily lives, a lifelong accumulation could presumably reach to a toxic level, jeopardizing neuronal function and brain health.Per- and polyfluoroalkyl substances (PFASs) are a group of man-made chemicals that have been widely used in consumer products around the world since the 1950s. They have been very widely used and closely linked to our daily lives, being used, for example, on fabrics to provide stain resistance, and on cookware to keep food from sticking to it. While PFAS compounds facilitate our lives, they have brought environmental challenges with them, mainly due to their broad application, vast numbers (there are thousands of fluoroalkyl chemical compounds), and due to a chain of linked carbon and fluorine atoms that result in very slow breakdown over time, a long lifespan (7). Due to its widespread use, humans have been widely exposed to these chemicals, many of which can now be found in blood and cerebrospinal fluid (CSF) samples. In combination with data from laboratory animals, it is suggested these chemicals may cause a series of health issues, as summarized in Figure 1 (7,8).In this issue, Delcourt and colleagues (9) present a small human study showing patients with high CSF PFASs correlate with AD. Here, using the CSF samples from 8 patients hospitalized with suspected normal pressure hydrocephalus, they checked levels of 18 of the most common PFAS molecules. PFASs were detected in all 8 CSF samples, and a correlation was seen between high PFOS (perfluorooctane sulfonate) and cognitive impairment among the tested individuals. This discovery brings with it a sense of urgency in reducing exposure to PFASs in our daily lives and highlights the risks that it may bring in terms of our brain health. As this is a small-size proof-of-concept study, further large-size clinical validation and underlying molecular investigation are needed.E.F.F. is supported by Cure Alzheimer’s Fund (#282952), HELSE SØR-ØST (#2020001, #2021021, #2023093), the Research Council of Norway (#262175, #334361), Molecule AG/VITADAO (#282942), NordForsk Foundation (#119986), the National Natural Science Foundation of China (#81971327), Akershus University Hospital (#269901, #261973, #262960), the Civitan Norges Forskningsfond for Alzheimers sykdom (#281931), the Czech Republic-Norway KAPPA programme (with Martin Vyhnálek, #TO01000215), the Rosa sløyfe/Norwegian Cancer Society & Norwegian Breast Cancer Society (#207819), and Wellcome Leap (#104617).E.F.F. is the co-owner of Fang-S Consultation AS (Organization number 931 410 717); he has an MTA with LMITO Therapeutics Inc. (South Korea), a CRADA arrangement with ChromaDex (United States), a commercialization agreement with Molecule AG/VITADAO; he is a consultant to Aladdin Healthcare Technologies (United Kingdom and Germany), the Vancouver Dementia Prevention Centre (Canada), Intellectual Labs (Norway), MindRank AI (China), and NYO3 (Norway and China). H-L.W. declares no conflict of interest.
研究领域:
神经科学
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环境健康
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医学
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DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2025
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IF 5.4
Shixiong Zhang,Xinjing Mao,Liping Chang,Mengnan Li,Cong Wei,Hongrong Li,Xiaogang Shen,Kunxu Niu,Runtao Zhang,Yuning Jiang,Xuan Lu,Yahui Song,Liangxing Zhou,Lini Gao,Zhiqin Zhao,Liying Niu,Qian Yang,Yunlong Hou,Yiling Wu
Ethnopharmacological relevance Bazi Bushen Capsule (BZBS), a traditional Chinese medicine formulation composed of multiple bioactive herbal components, has been validated in multicenter randomized double-blind controlled trials for its potent anti-aging properties. Previous studies from our group have demonstrated that BZBS effectively restores gut microbiota homeostasis and attenuates the impairment of intestinal barrier function, thereby ameliorating age-related cognitive decline. However, the specific molecular mechanisms by which BZBS modulates key microbial-metabolite networks to delay brain aging remain poorly understood and warrant further investigation. Aim of the study This study aims to elucidate the key microbiota-metabolite networks through which BZBS improves cognitive function and delays brain aging in senescence-accelerated mouse-prone 8 (SAMP8) mice. Materials and methods Eight-week-old male SAMP8 mice were used as experimental models, randomly divided into Model, BZ-low (0.5 g/kg/d BZBS), BZ-high (1 g/kg/d BZBS), and RAPA (2 mg/kg/d rapamycin) groups. Senescence-accelerated mouse resistant 1 (SAMR1) mice served as the control group. Cognitive function was assessed using the Barnes Maze test and the three-chamber social test. The structural damage and pathological changes in the brain tissue were evaluated through transcranial Doppler, micro-computed tomography, Nissl staining, and Western blot analysis. Next, the intestinal barrier function was detected by hematoxylin-eosin (HE) staining, periodic acid-Schiff (PAS) staining, and immunofluorescence (IF) staining. Characteristic bacteria were identified by 16S rRNA sequencing, and metabolomic profiling was performed using non-targeted metabolomics. Akkermansia muciniphila (Akk) was cultured, and fecal microbiota transplantation (FMT) was employed to evaluate its contribution to intestinal barrier function. Results The study revealed that BZBS therapy not only enhances cognitive capabilities but also restores the intestinal barrier function. Akk was identified as a key regulatory agent mediating the therapeutic effects of BZBS. BZBS administration significantly increased the abundance of Akk and modulated its metabolite profile, particularly components associated with spermidine, thereby reinforcing the intestinal barrier and mitigating age-related cognitive decline. Furthermore, this study demonstrated that Akk, administered via fecal microbiota transplantation, alleviated dextran sulfate sodium (DSS)-induced colitis.. Conclusion The results showed that BZBS capsule, a traditional Chinese medicine, may delay brain aging in SAMP8 mice by modulating Akk and its spermidine production.
研究领域:
民族药理学
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微生物组学
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代谢组学
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神经科学
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产品关联
DOI
PubMed
高影响因子
PHYTOTHERAPY RESEARCH
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2025
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IF 6.3
Minghao Fan,Yudi Jiang,Chao Cai,Zhe Wang,Lu Chen,Shumin Hu,Xin Zhang,Hua Yin,Zhonghua Qian,Shuli Huang,Jiachen Yang
Depression often develops in young individuals and is linked to complications like cognitive impairment. Conventional antidepressants show limited efficacy in restoring cognitive function and may cause adverse effects. Green tea, a safe and health-promoting beverage, offers various health benefits. This study investigated the effects of long-term green tea consumption on stress-induced depression-like behavior and mild cognitive impairment in animal models. We established a rodent model of mild depression and studied the effects of green tea on depression-like behavior and cognitive impairment through comprehensive evaluation, including behavioral assessments, neurotransmitter quantification, gene and protein expression analysis, blood metabolite profiling, and gut microbiota characterization. Results demonstrated significant improvements in mood, long-term memory, and sterol and glycerophospholipid metabolism. Green tea repaired the intestinal barrier and upregulated genes vital for tight junctions and mucin production. It also enhanced gut microbiota composition, reducing the Firmicutes-to-Bacteroidetes ratio and promoting beneficial bacteria such as NK4A136 , Muribaculum , and Gordonibacter . These microbiota changes improved liver lipid metabolism and alleviated depressive symptoms. Green tea effectively mitigates depression-like behavior and cognitive deficits by modulating the gut-liver-brain axis.
研究领域:
神经科学
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营养学
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微生物学
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产品关联
DOI
PubMed
高影响因子
Foods
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2025
·Vol. 14
·期 5
·870
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IF 5.1
Dongying Chen,Xin Bi,Qian Feng,Yong Sun
In this study, the impact of lentil hull soluble dietary fibers (SDFs) on colitis and behavioral deficits in mice was assessed. Structural characterizations of SDFs confirmed that cellulase-modified soluble dietary fiber exhibited better physicochemical properties: more porous microstructure; similar polysaccharide structure; more stable particle size distribution; higher crystallinity; better adsorption capacity; and lower viscosity. Additionally, we explored its potential cognitive benefits via the gut-brain axis by behavioral tests, histopathology, 16S rRNA sequencing, gas chromatography and metabolomics analysis. The results showed that SDFs significantly improved inflammatory symptoms in colon and brain and cognitive behaviors. LSDF had better efficacy than HSDF. LSDF intervention decreased the harmful bacteria abundance (Bacteroides,FlexispiraandEscherichia, etc.) and increased beneficial bacteria abundance (AggregatibacterandHelicobacter, etc.). LSDF also affected brain metabolites through the sphingolipid metabolism. Spearman correlation analysis showed that there was a positive correlation between harmful bacteria with inflammatory factors (LPS, IL-1β, IL-6, and TNF-α, etc.) and sphingolipid metabolites, while beneficial bacteria were positively correlated with brain-derived neurotrophic factor (BDNF), IL-10, and cognitive behavior. This study highlights the value of SDFs in future diet-based therapeutic strategies targeting gut-brain interactions.
研究领域:
营养学
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微生物学
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神经科学
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产品关联
DOI
PubMed
高影响因子
FOOD RESEARCH INTERNATIONAL
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2025
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IF 8
Qian Zhao,Peilin Yang,Xiaolei Wang,Zhiyue Ye,Zhenzhen Xu,Jianle Chen,Shiguo Chen,Xingqian Ye,Huan Cheng
Citrus flavors are globally popular in food industry, yet research on the perceptual preferences of various citrus flavors is limited. Based on the subjective sensory evaluation, this study introduces a novel sensory analysis approach, using electroencephalography (EEG), to objectively measure the sensory and cognitive responses to nine citrus flavors, including d -limonene, concentrated (H-) and original essential oils of sweet orange (SEO), bergamot EO (BEO), lemon EO (LEO), and grapefruit EO (GEO). Results revealed that δ (0.5–4 Hz) and α (8–13 Hz) waves activity predominated in brain responses to citrus flavor, with greater activity observed in frontal and central regions compared to other areas. Sniffing citrus EOs triggered more complex and dynamic electrical activity than d -limonene, indicated by higher power density across all frequency bands (0.1-30 Hz). Interestingly, while the original citrus EOs were associated with higher self-reported acceptability, the concentrated forms elicited greater brain responses. Specifically, H-SEO and L-LEO eliciting significantly greater δ and α wave activity in the prefrontal region than their original forms ( P < 0.05). A preliminary correlation was observed between brain laterality in α waves power and acceptability scores of citrus flavor, with δ waves power in the prefrontal region further demonstrating an effective reflection of self-reported acceptability scores for SEO and LEO stimuli. This is the first EEG-based study to compare brain responses to different citrus flavors, providing important implications for the food industry in optimizing product formulations and enhancing consumer experiences.
研究领域:
食品科学
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神经科学
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产品关联
DOI
PubMed
高影响因子
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
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2024
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IF 4.2
Xiaochun Zhao,Xueting Wang,Ziyang Xu,Xiaohan Chang,Yue Tian
Perioperative neurocognitive disorders (PNDs) are common neurological complications after anesthesia in the elderly. Protein tyrosine phosphatase non-receptor type 2 (PTPN2) regulates signal transducer and activator of transcription protein 3 (STAT3) signaling to control inflammation in certain organs, but its role in PNDs remains unknown. Herein, we constructed a PND model in 18-month-old rats by treating them with sevoflurane. PND rats developed neuroinflammation, along with a significant decrease in PTPN2 expression and a rise in STAT3 phosphorylation in the hippocampus. Ptpn2 overexpression alleviated the behavioral disorders of PND rats, ameliorated neuronal injury, inhibited neuroinflammation, inflammasome activation, microglial activation, and microglial phenotype switching. Similar results were observed in sevoflurane-treated HMC3 microglia with PTPN2 overexpression, while PTPN2 silencing showed the opposite results. Additionally, PTPN2 seems to be a target of T-box transcription factor 2 (TBX2). These results contribute to the evidence supporting the idea that PTPN2 is a regulatory factor in PND progression.
研究领域:
神经科学
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药理学
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分子生物学
✓ 已验证
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）