Gamma-glutamyl transferase 5 overexpression in cerebrovascular endothelial cells improves brain pathology,cognition,and behavior in APP/PS1 mice

In patients with Alzheimer’s disease,gamma-glutamyl transferase 5(GGT5)expression has been observed to be downregulated in cerebrovascular endothelial cells.However,the functional role of GGT5 in the development of Alzheimer’s disease remains unclear.This study aimed to explore the effect of GGT5 on cognitive function and brain pathology in an APP/PS1 mouse model of Alzheimer’s disease,as well as the underlying mechanism.We observed a significant reduction in GGT5 expression in two in vitro models of Alzheimer’s disease(Aβ_(1-42)-treated hCMEC/D3 and bEnd.3 cells),as well as in the APP/PS1 mouse model.Additionally,injection of APP/PS1 mice with an adeno-associated virus encoding GGT5 enhanced hippocampal synaptic plasticity and mitigated cognitive deficits.Interestingly,increasing GGT5 expression in cerebrovascular endothelial cells reduced levels of both soluble and insoluble amyloid-βin the brains of APP/PS1 mice.This effect may be attributable to inhibition of the expression ofβ-site APP cleaving enzyme 1,which is mediated by nuclear factor-kappa B.Our findings demonstrate that GGT5 expression in cerebrovascular endothelial cells is inversely associated with Alzheimer’s disease pathogenesis,and that GGT5 upregulation mitigates cognitive deficits in APP/PS1 mice.These findings suggest that GGT5 expression in cerebrovascular endothelial cells is a potential therapeutic target and biomarker for Alzheimer’s disease.

Impact of propofol and sevoflurane anesthesia on cognition and emotion in gastric cancer patients undergoing radical resection

BACKGROUND Propofol and sevoflurane are commonly used anesthetic agents for maintenance anesthesia during radical resection of gastric cancer.However,there is a debate concerning their differential effects on cognitive function,anxiety,and depression in patients undergoing this procedure.AIM To compare the effects of propofol and sevoflurane anesthesia on postoperative cognitive function,anxiety,depression,and organ function in patients undergoing radical resection of gastric cancer.METHODS A total of 80 patients were involved in this research.The subjects were divided into two groups:Propofol group and sevoflurane group.The evaluation scale for cognitive function was the Loewenstein occupational therapy cognitive assessment(LOTCA),and anxiety and depression were assessed with the aid of the self-rating anxiety scale(SAS)and self-rating depression scale(SDS).Hemodynamic indicators,oxidative stress levels,and pulmonary function were also measured.RESULTS The LOTCA score at 1 d after surgery was significantly lower in the propofol group than in the sevoflurane group.Additionally,the SAS and SDS scores of the sevoflurane group were significantly lower than those of the propofol group.The sevoflurane group showed greater stability in heart rate as well as the mean arterial pressure compared to the propofol group.Moreover,the sevoflurane group displayed better pulmonary function and less lung injury than the propofol group.CONCLUSION Both propofol and sevoflurane could be utilized as maintenance anesthesia during radical resection of gastric cancer.Propofol anesthesia has a minimal effect on patients'pulmonary function,consequently enhancing their postoperative recovery.Sevoflurane anesthesia causes less impairment on patients'cognitive function and mitigates negative emotions,leading to an improved postoperative mental state.Therefore,the selection of anesthetic agents should be based on the individual patient's specific circumstances.

Design of a Landscape Device for Children from the Perspective of Embodied Cognition in the New Era

In recent years,embodied cognition has ushered in a new research upsurge in the academic field,and has become a hot topic in the field of cognitive psychology.In this paper,from the perspective of embodied cognition,the interaction ways of a landscape device for children were discussed to achieve a more real and harmonious interaction between children and scenes.The research data of embodied cognition used by children was analyzed,and the drawbacks and breakthrough points of current landscape devices for children were discussed.The core characteristics of children’s growth period were extracted to establish children’s interaction model and summarize the interactive design methods of landscape devices for children.Embodied cognition has become the most intuitive way for children to know and understand the environment,and plays a pivotal role in children’s growth.Based on embodied cognition principle and interactive behavior mode,the interactive design of a landscape device for children was studied,and three interactive design modes,including simple and convenient interaction mode,multi-sensory interaction mode and game natural interaction mode were summarized.On the basis of this research,relevant design practice and research were carried out to bring a new vision to the design of children’s landscape.

Impaired Cognition and Stroke Rehabilitation Outcomes: Are They Related?

Background: Stroke survivors who exhibit impaired cognition at admission to inpatient rehabilitation may experience participation challenges and poorer functional outcomes than those without impaired cognition. Differences in functional outcomes between stroke survivors with and without impaired cognition may be attributed to age, level of cognitive impairment, and severity of stroke. Materials and Methods: A retrospective secondary data analysis was conducted using health-related administrative data acquired from a Southwestern Ontario hospital’s stroke rehabilitation database. The aim was to explore potential linkages between post-stroke impaired cognition and functional gains, rehabilitation stays, and living settings after discharge from rehabilitation. Results: An aggregate sample of 393 males and 314 females subclassified as experiencing mild, moderate, and severe stroke was analyzed. At inpatient rehabilitation admission, 21.5% (n = 152) of these patients had no impaired cognition, 33.7% (n = 238) had mild impaired cognition, 22.2% (n = 157) had moderate impaired cognition, and 22.6% (n = 160) had severe impaired cognition. Cognitively impaired stroke patients were significantly (p 0.001) older, had (mostly) moderate to severe stroke with significantly (p = 0.012) more moderate cognitive impairment, had significantly (p 0.001) longer rehabilitation stays, and a high propensity for being discharged to longer-term care facilities compared to non-cognitively impaired patients. Conclusion: Presence of significant dissimilarity in rehabilitation stays and post-discharge destinations among stroke survivors with and without cognitive impairment is attributed to the age of the patient, level of cognitive impairment, and rigorous rehabilitation interventions.

Promotion of structural plasticity in area V2 of visual cortex prevents against object recognition memory deficits in aging and Alzheimer's disease rodents

Memory deficit,which is often associated with aging and many psychiatric,neurological,and neurodegenerative diseases,has been a challenging issue for treatment.Up till now,all potential drug candidates have failed to produce satisfa ctory effects.Therefore,in the search for a solution,we found that a treatment with the gene corresponding to the RGS14414protein in visual area V2,a brain area connected with brain circuits of the ventral stream and the medial temporal lobe,which is crucial for object recognition memory(ORM),can induce enhancement of ORM.In this study,we demonstrated that the same treatment with RGS14414in visual area V2,which is relatively unaffected in neurodegenerative diseases such as Alzheimer s disease,produced longlasting enhancement of ORM in young animals and prevent ORM deficits in rodent models of aging and Alzheimer’s disease.Furthermore,we found that the prevention of memory deficits was mediated through the upregulation of neuronal arbo rization and spine density,as well as an increase in brain-derived neurotrophic factor(BDNF).A knockdown of BDNF gene in RGS14414-treated aging rats and Alzheimer s disease model mice caused complete loss in the upregulation of neuronal structural plasticity and in the prevention of ORM deficits.These findings suggest that BDNF-mediated neuronal structural plasticity in area V2 is crucial in the prevention of memory deficits in RGS14414-treated rodent models of aging and Alzheimer’s disease.Therefore,our findings of RGS14414gene-mediated activation of neuronal circuits in visual area V2 have therapeutic relevance in the treatment of memory deficits.

Exploration and Practice of Life Education Curriculum Based on Embodied Cognition Theory

In recent years,the suicide rate of adolescents has been increasing year by year,and life and health problems have become the most important in education.It is urgent to promote the construction of the curriculum of life education effectively.In view of the“vacuity”and“fragmented”state of traditional life education,this paper combs the teaching objectives,teaching contents,teaching methods,and teaching evaluation of life education from the perspective of embodied cognition theory,to explore the construction of positive experience of life education curriculum.

Research on Children’s Game Activity Design Strategies Based on Embodied Cognition Theory

Edutainment,in the kindergarten education stage,emphasizes the game as the basic activity and combines the content of education with the form of the game,thus it also forms the educational method of gamification teaching.Through investigation and analysis,it is found that the current kindergarten game activity design has the problem of improper combination of educational content and game form.The current kindergarten game activity design has problems such as stereotypes,children’s lack of active learning opportunities in activities,teachers’insufficient theoretical understanding,inappropriate teacher guidance methods,and so on.Embodied cognition theory attaches importance to the important role of the body in the development of cognition,provides new guidance for classroom teaching,and opens up a new path for classroom teaching reform.Based on the perspective of embodied cognition theory,the concept of body and mind integration should be adhered to in kindergarten teaching with games as the basic activity,experiential teaching situation should be created,children’s subjective experience should be respected,and games and interactions should be designed to promote children’s physical and mental participation,thus laying a foundation for the realization of children’s individual freedom,autonomy,and all-round development.Therefore,this paper aims at the existing problems in the current kindergarten gamification teaching and discusses the design strategy of children’s game activities based on embodied cognition theory.

轻度认知障碍老人与认知正常老人在不同单双任务下姿势控制能力的差异性

背景:老年人由于轻度认知障碍而引起姿势控制能力下降,导致跌倒风险增高。双任务是在接近真实生活场景下评估认知与姿势控制能力关系的主要研究范式,站立时足底压力中心位移样本熵可代表姿势控制的复杂程度。目的:基于压力中心位移样本熵分析轻度认知障碍老年人与认知正常老年人在姿势控制-空间工作记忆任务中姿势稳定性特征及控制策略的差异,探究认知功能损伤对站立姿势控制能力影响。方法:筛选出符合条件的16名轻度认知障碍老年人和17名认知正常老年人为研究对象,老年人分别完成5种测试任务,包括空间工作记忆、双脚平衡站立、Romberg站立、双脚平衡站立-空间工作记忆双任务、Romberg站立-空间工作记忆双任务,每个任务有效完成3次。使用Kistler三维测力台采集足底压力中心数据,测试指标包括认知行为学指标(认知得分与反应时长)、动力学指标(压力中心位移及样本熵)。结果与结论:①轻度认知障碍老年人在执行空间工作记忆任务时认知得分最大、反应时间最短,双脚平衡站立-空间工作记忆双任务居中,Romberg站立-空间工作记忆双任务认知得分最小、反应时长最长,任务间比较差异均有显著性意义(P<0.05);②与双脚平衡站立、Romberg站立任务相比,轻度认知障碍老年人在执行双任务时压力中心前后、内外方向位移显著更大,压力中心前后、内外方向位移样本熵值显著更小(P<0.05);③在空间工作记忆任务下,轻度认知障碍老年人与认知正常老年人的认知得分、反应时长差异均无显著性意义(P>0.05);在两种双任务下,与认知正常老年人相比,轻度认知障碍老年人的认知得分更小、反应时长更长(P<0.05),同时轻度认知障碍老年人压力中心前后、内外方向位移更大,压力中心前后、内外方向位移样本熵值更小(P<0.05);④结果表明:与认知正常老年人相比,轻度认知障碍老年人在执行双任务时姿势控制复杂度降低,系统适应性较差,自动调控能力下降,更容易受到空间工作记忆干扰,跌倒风险增大。

城市老年人抑郁与认知功能的相关性及性别差异研究

背景我国人口老龄化问题日趋严重,抑郁是老年人群中较为常见的精神疾病之一,可导致显著的残疾和死亡风险增加。研究发现抑郁与认知障碍之间关联密切,并且这种关系可能受到性别的影响。在老年人群中,抑郁与认知功能及不同认知领域之间相关性的性别差异尚不明确。目的对城市老年人抑郁和认知功能状况进行调查,并分析抑郁与认知功能的相关性及性别差异。方法2022年9—10月采用分层抽样方法,选取安徽省合肥市某社区的65岁及以上老年居民作为调查对象。收集其一般资料,采用老年抑郁量表(GDS)、痴呆简易筛查量表(BSSD)分别对抑郁和认知功能状况进行评估,探讨老年人抑郁的相关因素,并分析抑郁、性别因素及二者的交互作用对认知功能的影响。结果共纳入328名老年人,抑郁的总体检出率为14.9%。回归分析结果显示,饮酒(OR=0.362,95%CI=0.155~0.847)、与子女居住(OR=2.445,95%CI=1.021~5.853)是抑郁的独立相关因素(P<0.05)。析因设计的方差分析显示,抑郁老年人的BSSD总分及语言(命令)理解、计算/注意、地点定向、时间定向和即刻记忆因子分均低于非抑郁老年人(P<0.05)。女性BSSD总分及常识/图片理解和地点定向因子分均低于男性,而语言(命令)理解得分高于男性(P<0.05)。抑郁与性别在常识/图片理解、语言(命令)理解和地点定向上的交互作用显著(P<0.05)。结论城市老年人抑郁风险较高,合并抑郁的老年人可能存在一定的认知功能减退,并伴有性别差异。应加强关注老年人抑郁和痴呆等精神问题,尤其是针对女性老年群体,有必要制定个体化的综合干预措施,提高老年人心理健康水平和生活质量。

Decreased levels of phosphorylated synuclein in plasma are correlated with poststroke cognitive impairment

Poststro ke cognitive impairment is a major secondary effect of ischemic stroke in many patients;however,few options are available for the early diagnosis and treatment of this condition.The aims of this study were to(1)determine the specific relationship between hypoxic andα-synuclein during the occur of poststroke cognitive impairment and(2)assess whether the serum phosphorylatedα-synuclein level can be used as a biomarker for poststro ke cognitive impairment.We found that the phosphorylatedα-synuclein level was significantly increased and showed pathological aggregation around the cerebral infa rct area in a mouse model of ischemic stroke.In addition,neuronalα-synuclein phosphorylation and aggregation were observed in the brain tissue of mice subjected to chronic hypoxia,suggesting that hypoxia is the underlying cause ofα-synuclein-mediated pathology in the brains of mice with ischemic stroke.Serum phosphorylatedα-synuclein levels in patients with ischemic stroke were significantly lower than those in healt hy subjects,and were positively correlated with cognition levels in patients with ischemic stroke.Furthermore,a decrease in serum high-density lipoprotein levels in stroke patie nts was significantly correlated with a decrease in phosphorylatedα-synuclein levels.Although ischemic stroke mice did not show significant cognitive impairment or disrupted lipid metabolism 14 days after injury,some of them exhibited decreased cognitive function and reduced phosphorylatedα-synuclein levels.Taken together,our results suggest that serum phosphorylatedα-synuclein is a potential biomarker for poststroke cognitive impairment.

Small heat shock protein B8:from cell functions to its involvement in diseases and potential therapeutic applications

Heat shock protein family B(small)member 8(HSPB8)is a 22 kDa ubiquitously expressed protein belonging to the family of small heat shock proteins.HSPB8 is involved in various cellular mechanisms mainly related to proteotoxic stress response and in other processes such as inflammation,cell division,and migration.HSPB8 binds misfolded clients to prevent their aggregation by assisting protein refolding or degradation through chaperone-assisted selective autophagy.In line with this function,the pro-degradative activity of HSPB8 has been found protective in several neurodegenerative and neuromuscular diseases characterized by protein misfolding and aggregation.In cancer,HSPB8 has a dual role being capable of exerting either a pro-or an anti-tumoral activity depending on the pathways and factors expressed by the model of cancer under investigation.Moreover,HSPB8 exerts a protective function in different diseases by modulating the inflammatory response,which characterizes not only neurodegenerative diseases,but also other chronic or acute conditions affecting the nervous system,such as multiple sclerosis and intracerebellar hemorrhage.Of note,HSPB8 modulation may represent a therapeutic approach in other neurological conditions that develop as a secondary consequence of other diseases.This is the case of cognitive impairment related to diabetes mellitus,in which HSPB8 exerts a protective activity by assuring mitochondrial homeostasis.This review aims to summarize the diverse and multiple functions of HSPB8 in different pathological conditions,focusing on the beneficial effects of its modulation.Drug-based and alternative therapeutic approaches targeting HSPB8 and its regulated pathways will be discussed,emphasizing how new strategies for cell and tissue-specific delivery represent an avenue to advance in disease treatments.

Decoding molecular mechanisms:brain aging and Alzheimer's disease

The complex morphological,anatomical,physiological,and chemical mechanisms within the aging brain have been the hot topic of research for centuries.The aging process alters the brain structure that affects functions and cognitions,but the worsening of such processes contributes to the pathogenesis of neurodegenerative disorders,such as Alzheimer's disease.Beyond these observable,mild morphological shifts,significant functional modifications in neurotransmission and neuronal activity critically influence the aging brain.Understanding these changes is important for maintaining cognitive health,especially given the increasing prevalence of age-related conditions that affect cognition.This review aims to explore the age-induced changes in brain plasticity and molecular processes,differentiating normal aging from the pathogenesis of Alzheimer's disease,thereby providing insights into predicting the risk of dementia,particularly Alzheimer's disease.

Nanocarrier-mediated siRNA delivery:a new approach for the treatment of traumatic brain injury-related Alzheimer's disease

Traumatic brain injury and Alzheimer's disease share pathological similarities,including neuronal loss,amyloid-βdeposition,tau hyperphosphorylation,blood-brain barrier dysfunction,neuroinflammation,and cognitive deficits.Furthermore,traumatic brain injury can exacerbate Alzheimer's disease-like pathologies,potentially leading to the development of Alzheimer's disease.Nanocarriers offer a potential solution by facilitating the delive ry of small interfering RNAs across the blood-brain barrier for the targeted silencing of key pathological genes implicated in traumatic brain injury and Alzheimer's disease.U nlike traditional approaches to neuro regeneration,this is a molecula r-targeted strategy,thus avoiding non-specific drug actions.This review focuses on the use of nanocarrier systems for the efficient and precise delive ry of siRNAs,discussing the advantages,challenges,and future directions.In principle,siRNAs have the potential to target all genes and non-targetable protein s,holding significant promise for treating various diseases.Among the various therapeutic approaches currently available for neurological diseases,siRNA gene silencing can precisely"turn off"the expression of any gene at the genetic level,thus radically inhibiting disease progression;however,a significant challenge lies in delivering siRNAs across the blood-brain barrier.Nanoparticles have received increasing attention as an innovative drug delive ry tool fo r the treatment of brain diseases.They are considered a potential therapeutic strategy with the advantages of being able to cross the blood-brain barrier,targeted drug delivery,enhanced drug stability,and multifunctional therapy.The use of nanoparticles to deliver specific modified siRNAs to the injured brain is gradually being recognized as a feasible and effective approach.Although this strategy is still in the preclinical exploration stage,it is expected to achieve clinical translation in the future,creating a new field of molecular targeted therapy and precision medicine for the treatment of Alzheimer's disease associated with traumatic brain injury.

Acute and chronic excitotoxicity in ischemic stroke and late-onset Alzheimer's disease

Stroke and Alzheimer's disease are common neurological disorders and often occur in the same individuals.The comorbidity of the two neurological disorders represents a grave health threat to older populations.This review presents a brief background of the development of novel concepts and their clinical potentials.The activity of glutamatergic N-methyl-D-aspartate receptors and N-methyl-D-aspartate receptor-mediated Ca^(2+)influx is critical for neuronal function.An ischemic insult induces prompt and excessive glutamate release and drastic increases of intracellular Ca^(2+)mainly via N-methyl-D-aspartate receptors,particularly of those at the extrasynaptic site.This Ca^(2+)-evoked neuronal cell death in the ischemic core is dominated by necrosis within a few hours and days known as acute excitotoxicity.Furthermore,mild but sustained Ca^(2+)increases under neurodegenerative conditions such as in the distant penumbra of the ischemic brain and early stages of Alzheimer's disease are not immediately toxic,but gradually set off deteriorating Ca^(2+)-dependent signals and neuronal cell loss mostly because of activation of programmed cell death pathways.Based on the Ca^(2+)hypothesis of Alzheimer's disease and recent advances,this Ca^(2+)-activated“silent”degenerative excitotoxicity evolves from years to decades and is recognized as a unique slow and chronic neuropathogenesis.The N-methyl-D-aspartate receptor subunit GluN3A,primarily at the extrasynaptic site,serves as a gatekeeper for the N-methyl-D-aspartate receptor activity and is neuroprotective against both acute and chronic excitotoxicity.Ischemic stroke and Alzheimer's disease,therefore,share an N-methyl-D-aspartate receptor-and Ca^(2+)-mediated mechanism,although with much different time courses.It is thus proposed that early interventions to control Ca^(2+)homeostasis at the preclinical stage are pivotal for individuals who are susceptible to sporadic late-onset Alzheimer's disease and Alzheimer's disease-related dementia.This early treatment simultaneously serves as a preconditioning therapy against ischemic stroke that often attacks the same individuals during abnormal aging.

Recombinant chitinase-3-like protein 1 alleviates learning and memory impairments via M2 microglia polarization in postoperative cognitive dysfunction mice

Postoperative cognitive dysfunction is a seve re complication of the central nervous system that occurs after anesthesia and surgery,and has received attention for its high incidence and effect on the quality of life of patients.To date,there are no viable treatment options for postoperative cognitive dysfunction.The identification of postoperative cognitive dysfunction hub genes could provide new research directions and therapeutic targets for future research.To identify the signaling mechanisms contributing to postoperative cognitive dysfunction,we first conducted Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the Gene Expression Omnibus GSE95426 dataset,which consists of mRNAs and long non-coding RNAs differentially expressed in mouse hippocampus3 days after tibial fracture.The dataset was enriched in genes associated with the biological process"regulation of immune cells,"of which Chill was identified as a hub gene.Therefore,we investigated the contribution of chitinase-3-like protein 1 protein expression changes to postoperative cognitive dysfunction in the mouse model of tibial fractu re surgery.Mice were intraperitoneally injected with vehicle or recombinant chitinase-3-like protein 124 hours post-surgery,and the injection groups were compared with untreated control mice for learning and memory capacities using the Y-maze and fear conditioning tests.In addition,protein expression levels of proinflammatory factors(interleukin-1βand inducible nitric oxide synthase),M2-type macrophage markers(CD206 and arginase-1),and cognition-related proteins(brain-derived neurotropic factor and phosphorylated NMDA receptor subunit NR2B)were measured in hippocampus by western blotting.Treatment with recombinant chitinase-3-like protein 1 prevented surgery-induced cognitive impairment,downregulated interleukin-1βand nducible nitric oxide synthase expression,and upregulated CD206,arginase-1,pNR2B,and brain-derived neurotropic factor expression compared with vehicle treatment.Intraperitoneal administration of the specific ERK inhibitor PD98059 diminished the effects of recombinant chitinase-3-like protein 1.Collectively,our findings suggest that recombinant chitinase-3-like protein 1 ameliorates surgery-induced cognitive decline by attenuating neuroinflammation via M2 microglial polarization in the hippocampus.Therefore,recombinant chitinase-3-like protein1 may have therapeutic potential fo r postoperative cognitive dysfunction.

Enhanced autophagic clearance of amyloid-βvia histone deacetylase 6-mediated V-ATPase assembly and lysosomal acidification protects against Alzheimer's disease in vitro and in vivo

Recent studies have suggested that abnormal acidification of lysosomes induces autophagic accumulation of amyloid-βin neurons,which is a key step in senile plaque formation.Therefore,resto ring normal lysosomal function and rebalancing lysosomal acidification in neurons in the brain may be a new treatment strategy for Alzheimer's disease.Microtubule acetylation/deacetylation plays a central role in lysosomal acidification.Here,we show that inhibiting the classic microtubule deacetylase histone deacetylase 6 with an histone deacetylase 6 shRNA or thehistone deacetylase 6 inhibitor valproic acid promoted lysosomal reacidification by modulating V-ATPase assembly in Alzheimer's disease.Fu rthermore,we found that treatment with valproic acid markedly enhanced autophagy.promoted clearance of amyloid-βaggregates,and ameliorated cognitive deficits in a mouse model of Alzheimer's disease.Our findings demonstrate a previously unknown neuroprotective mechanism in Alzheimer's disease,in which histone deacetylase 6 inhibition by valproic acid increases V-ATPase assembly and lysosomal acidification.

Gut microbiota-astrocyte axis: new insights into age-related cognitive decline

With the rapidly aging human population,age-related cognitive decline and dementia are becoming increasingly prevalent worldwide.Aging is considered the main risk factor for cognitive decline and acts through alterations in the composition of the gut microbiota,microbial metabolites,and the functions of astrocytes.The microbiota–gut–brain axis has been the focus of multiple studies and is closely associated with cognitive function.This article provides a comprehensive review of the specific changes that occur in the composition of the gut microbiota and microbial metabolites in older individuals and discusses how the aging of astrocytes and reactive astrocytosis are closely related to age-related cognitive decline and neurodegenerative diseases.This article also summarizes the gut microbiota components that affect astrocyte function,mainly through the vagus nerve,immune responses,circadian rhythms,and microbial metabolites.Finally,this article summarizes the mechanism by which the gut microbiota–astrocyte axis plays a role in Alzheimer’s and Parkinson’s diseases.Our findings have revealed the critical role of the microbiota–astrocyte axis in age-related cognitive decline,aiding in a deeper understanding of potential gut microbiome-based adjuvant therapy strategies for this condition.

身体活动与执行功能领域研究主题的动态演化

背景:身体活动与执行功能领域的相关研究不断涌现,目前尚未有学者使用可视化工具探讨这一领域研究主题的动态演化路径。目的:通过文献计量学方法,探究身体活动与执行功能领域研究主题的动态演化过程,从而理清其发展状态及知识结构的变化。方法:通过检索式:TS=(“Physical activity”AND“Executive function*”)OR TS=(Exercise AND“Executive function*”)检索Web of Science数据库,依照纳入排除标准选取4386篇相关文献为研究内容,利用SciMAT软件进行可视化分析。结果与结论:身体活动与执行功能领域的研究呈现蓬勃发展态势,相关研究日趋深入,未来发展空间较大;该领域可分为执行功能、儿童、老年人和干预措施4个方向,并形成了11条主要演化路径;“运动技能”“生活方式”“有氧运动”和“干预措施”等主题可能是未来的研究重点,“青少年”和“老年人”群体是该领域研究的重点关注人群。

认知症污名的研究新进展

认知障碍又称认知症。随着人口老龄化进程的加快,受认知症和阿尔茨海默病影响的人群在不断增多。有关认知症的污名在国际社会被公认为普遍存在,但相关的研究却十分有限。本文通过梳理既往有关认知症污名的研究成果,发现有关认知症污名的定义和测量方式有待统一,有关经济欠发达地区的研究十分欠缺,能够进行因果推断的证据缺乏,干预研究的数量和质量均有很大的提升空间。对于认知症污名的研究,为打破传统污名研究领域中二元主体视角提供了难得的契机。同时,对认知症污名形成机制的讨论,也可以深化学界对标签理论和归因理论的探讨。

Viewing on similarities in metaphors in cross-cultural communication from the perspective of cognition

Modern cognitive linguistics claims that metaphor should not be studied simply as a rhetorical device of language, but be associated with mankind＇s cognitive process, because it reflects the relationship between language and thought and cognition. Owing to this common cognitive basis, metaphors of different languages and cultures have some similarities. The specific examples of metaphors, both in English and Chinese, will be compared to find out their similarities, thus providing the evidence for the cognitive basis of metaphors.