The intersection of visual impairment and mental health has profound effects on quality of life and warrants attention from healthcare providers,educators,and policymakers.With 20 million children under the age of 14 ...The intersection of visual impairment and mental health has profound effects on quality of life and warrants attention from healthcare providers,educators,and policymakers.With 20 million children under the age of 14 affected globally,older adults also experience significant psychological impact including depression,anxiety,and cognitive impairment.The implications of vision-related challenges extend far beyond mere sight.Depression and anxiety,exacerbated by social isolation and reduced physical activity,underscore the need for comprehensive interventions that address both medical and psychosocial dimensions.By recognizing the profound impact of ocular morbidities like strabismus,myopia,glaucoma,and age-related macular degeneration on mental health and investing in effective treatments and inclusive practices,society can pave the way for a healthier,more equitable future for affected individuals.There is evidence that myopic children experience a higher prevalence of depressive symptoms compared to their normal peers,and interventions like the correction of strabismus can enhance psychological outcome-demonstrating the value of an integrated management approach.展开更多
Dementia is a growing global health burden,with mild cognitive impairment(MCI)serving as a critical transitional stage[1].Identifying the nutritional risk factors is crucial for prevention.While nutrition plays a key ...Dementia is a growing global health burden,with mild cognitive impairment(MCI)serving as a critical transitional stage[1].Identifying the nutritional risk factors is crucial for prevention.While nutrition plays a key role in preventing age-related diseases and staple foods are a major dietary source,existing research on cognitive function has predominantly emphasized whole-grain consumption.There is limited evidence regarding the effects of specific staple food types on MCI.展开更多
Background As the population in China rapidly ages,the prevalence of mild cognitive impairment(MCI)is increasing considerably.However,the causes of MCI vary.The continued lack of understanding of the various subtypes ...Background As the population in China rapidly ages,the prevalence of mild cognitive impairment(MCI)is increasing considerably.However,the causes of MCI vary.The continued lack of understanding of the various subtypes of MCI impedes the implementation of effective measures to reduce the risk of advancing to more severe cognitive diseases.Aims To estimate the prevalence and incidence rates of two MCI subtypes—amnestic MCI(aMCI)and vascular cognitive impairment without dementia(VCIND)—and to determine modifiable factors for them among older individuals in a multiregional Chinese cohort.Method This 1-year longitudinal study surveyed a random sample of participants aged≥60 years from a large,community-dwelling cohort in China.Baseline lifestyle data were self-reported,while vascular and comorbid conditions were obtained from medical records and physical examinations.In total,3514 and 2051 individuals completed the baseline and 1-year follow-up assessments,respectively.Logistic and linear regression analyses were used to identify the modifiable factors for MCI subtypes and predictors of cognitive decline,respectively.Results Among our participants,aMCI and VCIND demonstrated prevalence of 14.83%and 2.71%,respectively,and annual incidence(per 1000 person-years)of 69.6 and 10.6,respectively.The risk factor for aMCI was age,whereas its protective factors were high education level,tea consumption and physical activity.Moreover,VCIND risk factors were age,hypertension and depression.The presence of endocrine disease,cerebral trauma or hypertension was associated with a faster decline in cognition over 1 year.Conclusions MCI is a serious health problem in China that will only worsen as the population ages if no widespread interventions are implemented.Preventive strategies that promote brain activity and support healthy lifestyle choices are required.We identified modifiable factors for MCI in older individuals.The easy-to-adopt solutions such as tea consumption and physical activity can aid in preventing MCI.展开更多
Cognitive impairment is a particularly severe non-motor symptom of Parkinson's disease that significantly diminishes the quality of life of affected individuals.Identifying reliable biomarkers for cognitive impair...Cognitive impairment is a particularly severe non-motor symptom of Parkinson's disease that significantly diminishes the quality of life of affected individuals.Identifying reliable biomarkers for cognitive impairment in Parkinson's disease is essential for early diagnosis,prognostic assessments,and the development of targeted therapies.This review aims to summarize recent advancements in biofluid biomarkers for cognitive impairment in Parkinson's disease,focusing on the detection of specific proteins,metabolites,and other biomarkers in blood,cerebrospinal fluid,and saliva.These biomarkers can shed light on the multifaceted etiology of cognitive impairment in Parkinson's disease,which includes protein misfolding,neurodegeneration,inflammation,and oxidative stress.The integration of biofluid biomarkers with neuroimaging and clinical data can facilitate the development of predictive models to enhance early diagnosis and monitor the progression of cognitive impairment in patients with Parkinson's disease.This comprehensive approach can improve the existing understanding of the mechanisms driving cognitive decline and support the development of targeted therapeutic strategies aimed at modifying the course of cognitive impairment in Parkinson's disease.Despite the promise of these biomarkers in characterizing the mechanisms underlying cognitive decline in Parkinson's disease,further research is necessary to validate their clinical utility and establish a standardized framework for early detection and monitoring of cognitive impairment in Parkinson's disease.展开更多
Adult hippocampal neurogenesis is linked to memory formation in the adult brain,with new neurons in the hippocampus exhibiting greater plasticity during their immature stages compared to mature neurons.Abnormal adult ...Adult hippocampal neurogenesis is linked to memory formation in the adult brain,with new neurons in the hippocampus exhibiting greater plasticity during their immature stages compared to mature neurons.Abnormal adult hippocampal neurogenesis is closely associated with cognitive impairment in central nervous system diseases.Targeting and regulating adult hippocampal neurogenesis have been shown to improve cognitive deficits.This review aims to expand the current understanding and prospects of targeting neurogenesis in the treatment of cognitive impairment.Recent research indicates the presence of abnormalities in AHN in several diseases associated with cognitive impairment,including cerebrovascular diseases,Alzheimer's disease,aging-related conditions,and issues related to anesthesia and surgery.The role of these abnormalities in the cognitive deficits caused by these diseases has been widely recognized,and targeting AHN is considered a promising approach for treating cognitive impairment.However,the underlying mechanisms of this role are not yet fully understood,and the effectiveness of targeting abnormal adult hippocampal neurogenesis for treatment remains limited,with a need for further development of treatment methods and detection techniques.By reviewing recent studies,we classify the potential mechanisms of adult hippocampal neurogenesis abnormalities into four categories:immunity,energy metabolism,aging,and pathological states.In immunity-related mechanisms,abnormalities in meningeal,brain,and peripheral immunity can disrupt normal adult hippocampal neurogenesis.Lipid metabolism and mitochondrial function disorders are significant energy metabolism factors that lead to abnormal adult hippocampal neurogenesis.During aging,the inflammatory state of the neurogenic niche and the expression of aging-related microRNAs contribute to reduced adult hippocampal neurogenesis and cognitive impairment in older adult patients.Pathological states of the body and emotional disorders may also result in abnormal adult hippocampal neurogenesis.Among the current strategies used to enhance this form of neurogenesis,physical therapies such as exercise,transcutaneous electrical nerve stimulation,and enriched environments have proven effective.Dietary interventions,including energy intake restriction and nutrient optimization,have shown efficacy in both basic research and clinical trials.However,drug treatments,such as antidepressants and stem cell therapy,are primarily reported in basic research,with limited clinical application.The relationship between abnormal adult hippocampal neurogenesis and cognitive impairment has garnered widespread attention,and targeting the former may be an important strategy for treating the latter.However,the mechanisms underlying abnormal adult hippocampal neurogenesis remain unclear,and treatments are lacking.This highlights the need for greater focus on translating research findings into clinical practice.展开更多
Ischemic stroke has a higher survival rate and is more likely to result in cognitive impairment than hemorrhagic stroke.The primary pathological mechanism underlying cognitive impairment involves dysfunction of neural...Ischemic stroke has a higher survival rate and is more likely to result in cognitive impairment than hemorrhagic stroke.The primary pathological mechanism underlying cognitive impairment involves dysfunction of neural circuits and damage to specific brain regions.This review aims to investigate the role of the hippocampus in cognitive impairment following a stroke.A review of the literature suggests that the hippocampus is a metabolically active structure that is easily involved in various metabolic states,such as hypoxia and hypoglycaemia.The functional changes in hippocampal cells associated with poststroke cognitive impairment mainly manifest as neuronal apoptosis,impaired synaptic plasticity,and decreased neurogenesis.The primary pathological mechanism of poststroke cognitive impairment involves a complex cascade of reactions,including neuroinflammatory activation,bursts of oxidative stress,and neuronal apoptosis induced by mitochondrial dysfunction.Interventional drugs for cognitive impairment after cerebral ischemia include neuroprotective drugs,traditional Chinese medicines and their extracts,and stem cell therapies.Many of these drugs have unique advantages,including the inhibition of neuroinflammation,the prevention of apoptosis,and the promotion of neurogenesis.They hold great potential for the prevention and treatment of cognitive impairment following cerebral ischemia.However,most current studies are animal experiments,and relatively few clinical studies exist.In future research,emphasis should be placed on interventions for cognitive impairment following cerebral ischemia.These findings offer novel perspectives for the treatment of cognitive impairment after cerebral ischemia.Finally,the role of hippocampal cell dysfunction in other diseases associated with cognitive decline is briefly discussed.The aim of this review is to provide researchers with a comprehensive overview of the role of the hippocampus in cognitive impairment and its intervention strategies.展开更多
Background:The absence of effective animal models for sporadic Alzheimer's disease(AD)remains a pivotal barrier to therapy development.Because methanol metabolism produces endogenous formaldehyde,a neurotoxic agen...Background:The absence of effective animal models for sporadic Alzheimer's disease(AD)remains a pivotal barrier to therapy development.Because methanol metabolism produces endogenous formaldehyde,a neurotoxic agent linked to cognitive decline,this study investigated whether chronic,low-dose methanol exposure could recapitulate AD-like pathology and cognitive deficits in rhesus monkey,thereby establishing a nonhuman primate animal model driven by this environmental-metabolic insult.Methods:Adult rhesus monkeys received low-concentration methanol for 9 months.Behavioral tests for cognition,locomotion,sleep,and vision were conducted.Postmortem analyses involved histopathological examination,immunohistochemistry,immunofluorescence,and Western blot to evaluate neuronal integrity,microglial activation,and the expression of key proteins associated with AD(amyloid-β[Aβ],phosphorylated tau,TAR DNA-binding protein 43[TDP-43])and cellular stress(synaptic markers,mitochondrial fission,autophagy,and apoptosis-related proteins).Results:Chronic methanol exposure led to progressive cognitive and memory impairment without significant motor or visual deficits.Neuropathology revealed brain atrophy,neuronal loss,synaptic damage,microglial activation,and mitochondrial structural disorganization.Critically,the exposed animals exhibited hallmark AD-like molecular alterations,including increased Aβ deposition,tau hyperphosphorylation,and TDP-43 dysregulation.Furthermore,neurotoxicity was associated with elevated urinary formaldehyde,enhanced mitochondrial fission,increased autophagy,and elevated apoptosis.Conclusion:Chronic low-dose methanol exposure in rhesus monkeys recapitulates progressive cognitive deficits and AD-like neuropathological features.This model,driven by endogenous formaldehyde toxicity,effectively mimics key aspects of sporadic AD.Our findings shed light on the neurotoxic mechanisms of methanol and propose a reproducible and translationally relevant nonhuman primate model for studying AD pathogenesis and evaluating potential therapeutics.展开更多
The increasing global prevalence of mild cognitive impairment(MCI)necessitates a paradigm shift in early detection strategies.Conventional neuropsychological assessment methods,predominantly paper-and-pencil tests suc...The increasing global prevalence of mild cognitive impairment(MCI)necessitates a paradigm shift in early detection strategies.Conventional neuropsychological assessment methods,predominantly paper-and-pencil tests such as the Mini-Mental State Examination and the Montreal Cognitive Assessment,exhibit inherent limitations with respect to accessibility,administration burden,and sensitivity to subtle cognitive decline,particularly among diverse populations.This commentary critically examines a recent study that champions a novel approach:The integration of gait and handwriting kinematic parameters analyzed via machine learning for MCI screening.The present study positions itself within the broader landscape of MCI detection,with a view to comparing its advantages against established neuropsychological batteries,advanced neuroimaging(e.g.,positron emission tomography,magnetic resonance imaging),and emerging fluid biomarkers(e.g.,cerebrospinal fluid,blood-based assays).While the study demonstrates promising accuracy(74.44%area under the curve 0.74 with gait and graphic handwriting)and addresses key unmet needs in accessibility and objectivity,we highlight its cross-sectional nature,limited sample diversity,and lack of dual-task assessment as areas for future refinement.This commentary posits that kinematic biomarkers offer a distinctive,scalable,and ecologically valid approach to widespread MCI screening,thereby complementing existing methods by providing real-world functional insights.Future research should prioritize longitudinal validation,expansion to diverse cohorts,integration with multimodal data including dual-tasking,and the development of highly portable,artificial intelligence-driven solutions to achieve the democratization of early MCI detection and enable timely interventions.展开更多
Traditional clinical subtype classifications(such as amnestic and non-amnestic mild cognitive impairment)rely on subjective interpretations of overlapping patterns of performance on cognitive tests,which may lead to u...Traditional clinical subtype classifications(such as amnestic and non-amnestic mild cognitive impairment)rely on subjective interpretations of overlapping patterns of performance on cognitive tests,which may lead to unreliable categorization.A more precise and objective classification of mild cognitive impairment subtypes can be achieved through data-driven clustering techniques.However,because previous studies have not restricted their cohorts to patients who have mild cognitive impairment with the pathology of Alzheimer’s disease,the nature of cognitive variability and its impact on disease progression in a strictly defined biomarker-positive preclinical Alzheimer’s disease cohort remains unknown.We examined cognitive heterogeneity among participants with mild cognitive impairment due to Alzheimer’s disease and evaluated its prognostic utility.Neuropsychological test data from 389 patients with mild cognitive impairment in whom the cerebrospinal fluid biomarker confirmed Alzheimer’s disease were obtained from the Alzheimer’s Disease Neuroimaging Initiative cohorts.Principal component analysis and model-based clustering were used to identify cognitive profiles,which were then validated through a 100-time bootstrap analysis.Pairwise comparisons tested for differences between the identified subgroups in participant characteristics,scores on cognitive and clinical outcomes,levels of cerebrospinal fluid biomarkers,and magnetic resonance imaging-derived brain volumes.Longitudinal analyses evaluated differences in rate of change of magnetic resonance imaging volumetric measurements and clinical outcomes over 48 months.Survival analysis assessed risk for conversion to dementia.Alpha-synuclein levels and white matter hyperintensity volumes were considered for sensitivity analysis.Two distinct cognitive profiles were identified:a“typical”group(56.04%of the sample)that demonstrated relatively poorer scores on memory testing than non-memory tests,and an“atypical”group(43.96%of the sample)with smaller differences between memory and non-memory measures,indicating a more uniform pattern of impairment across cognitive domains.While the groups had comparable levels of overall cognitive impairment and cerebrospinal fluid biomarkers of Alzheimer’s disease,the typical group displayed accelerated atrophy rates every 6 months across multiple brain regions(hippocampus:29.02 mm^(3),standard error[SE]=10.13,P=0.005;whole brain:1799.85 mm^(3),SE=781.57,P=0.023;entorhinal cortex:22.26 mm^(3),SE=11.15,P=0.048;fusiform gyrus:66.24 mm^(3),SE=28.53,P=0.021).Survival analysis revealed markedly higher dementia conversion risk(hazard ratio:1.70,95%confidence interval:1.27,2.27,P<0.001)and shorter progression time in the typical group.These findings persisted after controlling for comorbid pathologies.In conclusion,this data-driven approach identified two distinct cognitive subtypes of mild cognitive impairment due to Alzheimer’s disease that differed in their rates of clinical decline and neurodegeneration.These findings could be used to improve prognostic models and inform clinical trial stratification.展开更多
Sepsis-associated encephalopathy(SAE)is a severe neurological syndrome marked by widespread brain dysfunctions due to sepsis,yet the underlying mechanisms remain elusive.The current study,using a Lipopolysaccharide(LP...Sepsis-associated encephalopathy(SAE)is a severe neurological syndrome marked by widespread brain dysfunctions due to sepsis,yet the underlying mechanisms remain elusive.The current study,using a Lipopolysaccharide(LPS)-induced septic rat model,revealed the hyperphosphorylation of tau and cognitive impairments,accompanied by the release of inflammatory cytokines and activation of glial cells in the hippocampal dentate gyrus region of septic rats.Proteomic and bioinformatic analyses identified C-X-C motif chemokine ligand 10(CXCL10)as a central regulator of neuroinflammation.LPS triggered CXCL10 secretion in astrocytes,and astrocyte-conditioned medium from LPS-treated astrocytes induced tau hyperphosphorylation and synaptic deficits.Recombinant CXCL10 recapitulated these effects in vitro and in vivo.Blocking CXCL10–CXCR3 interaction reversed tau phosphorylation,synaptic impairment,and cognitive decline.Mechanistically,CXCL10–CXCR3 interaction activated CaMKII,driving tau hyperphosphorylation,while CaMKII inhibition restored synaptic protein levels.These findings establish CXCL10 as a key driver of tau pathology in SAE and suggest CXCL10–CXCR3 as a therapeutic target for sepsis-induced cognitive impairments.展开更多
Purpose: Individuals with mild cognitive impairment (MCI) frequently experience negative emotions, which are closely correlated with an accelerated rate of cognitive decline and the subsequent transition to a state of...Purpose: Individuals with mild cognitive impairment (MCI) frequently experience negative emotions, which are closely correlated with an accelerated rate of cognitive decline and the subsequent transition to a state of dementia. Despite networked cognitive training has been demonstrated to enhance cognitive function in MCI, its effectiveness for negative emotions is still unknown. This review aimed to exam the influences of networked cognitive training on negative emotions and quality of life in people with MCI. Methods: Searches for eligible studies were conducted using PubMed, Web of Science, EMBASE, Cochrane Library, Psyc INFO, CNKI, Wanfang database, VIP database, and Sinomed. The retrieval time limit was set from their inception to 17 December 2025. The articles were reviewed and extracted by two researchers, and their quality was evaluated using the Cochrane risk-of-bias assessment tool. Subsequently, a meta-analysis was carried out utilizing RevMan 5.4 software. Results: The review comprised 13 randomized controlled trials with 626 individuals. The meta-analysis demonstrated that networked cognitive training significantly improved depression (SMD = -0.36;95% CI [-0.73, -0.00];p = .050), anxiety (SMD = -0.32;95% CI [-0.57, -0.06];p < .050), and quality of life (MD = 2.54;95% CI [0.98, 4.10];p < .001). In terms of the comparison of apathy, the effect of intervention was unclear. Conclusions: From these meta-analysis results, networked cognitive training may help patients for MCI with their anxiety, depression, and overall quality of life. However, because there are so few randomized controlled trials available, the evidence regarding apathy is still ambiguous. More thorough randomized controlled trials with larger samples are necessary to verify the significance of networked cognitive training on apathy and to consolidate the findings.展开更多
Cognitive impairment is a complex neurodegenerative disorder,and increased homocysteine levels are recognized as a major risk factor for this condition.Epigenetic modifications,particularly histone acetylation,have be...Cognitive impairment is a complex neurodegenerative disorder,and increased homocysteine levels are recognized as a major risk factor for this condition.Epigenetic modifications,particularly histone acetylation,have been implicated in the progression of cognitive impairment;however,the mechanisms underlying hyperhomocysteinemia-induced cognitive impairment remain unclear.In this study,we developed an hyperhomocysteinemia-induced cognitive impairment model by feeding mice a high-methionine diet and conducted behavioral and molecular analyses to elucidate the mechanisms involved in cognitive impairment.Behavioral experiments revealed significant cognitive deficits and neuroinflammation accompanied by a marked decrease in histone H3 lysine 27 acetylation in the hippocampus and cortex.Furthermore,metabolomic profiling and chromatin immunoprecipitation sequencing demonstrated substantial shifts in the levels of homocysteine metabolites and identified histone H3 lysine 27 acetylation-targeted genes involved in synaptic long-term potentiation,including Gria1,Gria3,Grin2a,Grin2b,Slc1a1,Slc24a2,Ptk2b,and Src.RNA sequencing confirmed that hyperhomocysteinemia induced neurodegeneration.In vitro experiments confirmed that decreased histone H3 lysine 27 acetylation downregulates the expression of these target genes in homocysteine-treated HT-22 cells,thereby impairing synaptic plasticity.Collectively,these findings suggest that aberrant expression of long-term potentiation-related genes regulated by histone H3 lysine 27 acetylation is a key driver of hyperhomocysteinemia-induced cognitive impairment.Targeting histone H3 lysine 27 acetylation-mediated epigenetic dysregulation may be a promising therapeutic strategy,offering potential avenues for intervention in individuals with cognitive impairment and neurodegenerative disorders.展开更多
With the intensification of population aging in China,the problem of cognitive impairment in the elderly has become increasingly prominent,attracting widespread attention from all sectors of society.Geriatric cognitiv...With the intensification of population aging in China,the problem of cognitive impairment in the elderly has become increasingly prominent,attracting widespread attention from all sectors of society.Geriatric cognitive impairment is characterized by chronicity,which not only seriously threatens the health of the elderly and reduces their quality of life,but also imposes a heavy burden on families and society due to its long course.Attaching importance to and strengthening the chronic disease management of elderly cognitive impairment has profound significance for delaying disease progression,improving patients’quality of life,and reducing the burden of family care.Therefore,this paper first comprehensively understands elderly cognitive impairment by briefly elaborating on its definition and characteristics;on this basis,it focuses on exploring effective strategies for the chronic disease management of elderly cognitive impairment,hoping to provide new ideas and methods for the management of this condition and offer useful references for relevant clinical research and practice.展开更多
Neurodegenerative diseases,such as Alzheimer’s disease and Parkinson’s disease,are associated with cognitive impairment and impaired brain glucose metabolism,posing significant challenges for the public health.We pr...Neurodegenerative diseases,such as Alzheimer’s disease and Parkinson’s disease,are associated with cognitive impairment and impaired brain glucose metabolism,posing significant challenges for the public health.We previously demonstrated that cyanidin 3-O-β-galactoside(Cy3Gal)from black chokeberry alleviated cognitive impairment in aging mice through regulating brain energy metabolism in a direct way.However,the indirect mechanisms in mitigating brain glucose hypometabolism remain underexplored.Here,we utilized a bilaterally intracerebroventricular injection of streptozotocin(ICV/STZ,3 mg/kg bw)-induced brain glucose hypometabolism model to investigate the effects of Cy3Gal on cognitive impairment alleviation.Our findings revealed that Cy3Gal administration significantly improved memory deficit and cognitive impairment in ICV/STZ-administrated mice.Subsequently,Cy3Gal showed excellent abilities in inhibiting astrocyte overactivation,regulating neurotransmitters metabolism,and promoting synaptic plasticity.Furthermore,Cy3Gal enhanced brain glucose metabolism by improving glycolysis and the TCA cycle.Additionally,Cy3Gal modulated levels of gut microbiota-derived metabolites,including acetate,butyrate,histidine,glutamine,serine,valine and isoleucine,which were closely linked to brain glucose metabolism.The in vitro results further demonstrated that these metabolites played an important role in the neuron-astrocyte energy metabolism,which accounted for the alleviation of glucose hypometabolism.Overall,our findings suggest that Cy3Gal mitigates ICV/STZ-induced cognitive impairment by modulating gut microbiota-derived short-chain fatty acids and amino acids,which in turn improves brain glucose metabolism.展开更多
OBJECTIVE:To examine the differences in cognitive processing between patients with mild cognitive impairment(MCI)of different Traditional Chinese Medicine(TCM)syndrome types to provide evidence supporting the TCM typi...OBJECTIVE:To examine the differences in cognitive processing between patients with mild cognitive impairment(MCI)of different Traditional Chinese Medicine(TCM)syndrome types to provide evidence supporting the TCM typing of MCI.METHODS:Participants were screened using a battery of scales for spleen and kidney deficiency(SKD)/liver Qi stagnation(LQS)-type MCI or those without syndrome or normal control(NC).Following sex,age,and educational matching,behavioral and electroencephalographic data were recorded using the verbal N-back experimental paradigm.The data were then analyzed and compared with respect to the reaction time and correctness of the participants in each group,as well as the amplitude and latency of the event-related potential(ERP)components of P2,N2,and P3.RESULTS:There were no statistically significant differences in the accuracy or reaction times of the behavioral data of the groups.Regarding ERP data,the SKD group had a shorter P2 latency than the LQS and NC groups,while the latter two groups did not differ statistically.The SKD group had a shorter N2 latency than the NC group,while the SKD group did not differ from the LQS group.The SKD and LQS groups had a shorter P3 latency than the NC group.CONCLUSION:Our study offers objective evidence of the distinction between the types of TCM syndrome.Different types of TCM syndromes produce different disease mechanisms,resulting in brain damage with different presentations of cognitive impairment and cognitive processing characteristics.展开更多
Vascular cognitive impairment and dementia is a debilitating neurological disorder caused by chronic cerebral hypoperfusion,for which no effective causative treatments are currently available.Intermittent hypoxia has ...Vascular cognitive impairment and dementia is a debilitating neurological disorder caused by chronic cerebral hypoperfusion,for which no effective causative treatments are currently available.Intermittent hypoxia has been shown to enhance cerebral blood flow in mice,but its efficacy in a model of vascular cognitive impairment and dementia remains unclear.In this study,we established a mouse model of vascular cognitive impairment and dementia by bilateral carotid artery stenosis.Intermittent hypoxia was induced before and after this stenosis.We found that intermittent hypoxia increased cerebral blood flow,oxygen saturation,and microcirculation in the prefrontal cortex and hippocampus in the model mice,without causing neurovascular damage.Additionally,intermittent hypoxia significantly improved cognitive function in the mouse model of vascular cognitive impairment and dementia,with perconditioning showing greater efficacy than preconditioning.Improvements in cerebral microcirculation and blood flow were positively correlated with cognitive recovery.Even in a mouse model of vascular cognitive impairment and dementia with comorbidities induced by a high-fat,high-fructose diet,intermittent hypoxic perconditioning demonstrated protective effects on cognitive function.Proteomic analysis indicated that mitochondrial protection is a key mechanism,particularly through upregulating NDUFB8 expression and increasing the activity of mitochondrial complex I.These findings suggest that intermittent hypoxia is a potential non-invasive strategy for the prevention and treatment of vascular cognitive impairment and dementia.展开更多
According to the Japanese Ministry of Health,Labour,and Welfare,14.2%of people were aged>75 years in Japan in 2018,and this number continues to rise.With population aging,the incidence of congestive heart failure(C...According to the Japanese Ministry of Health,Labour,and Welfare,14.2%of people were aged>75 years in Japan in 2018,and this number continues to rise.With population aging,the incidence of congestive heart failure(CHF)is also increasing.[1–3]Reports have shown that the presence of cognitive impairment(CI)in patients with CHF is associated with poor prognosis,[4–6]and the degree of CI is related to CHF severity.展开更多
Objective:To examine the research trends and hotspots of the application of cognitive reserve in stroke cognitive impairment using CiteSpace and provide a reference for developing effective measures to reduce the inci...Objective:To examine the research trends and hotspots of the application of cognitive reserve in stroke cognitive impairment using CiteSpace and provide a reference for developing effective measures to reduce the incidence of cognitive impairment in these patients.Methods:Using CiteSpace software,a visual analysis of 860 included articles related to cognitive reserve in stroke cognitive impairment patients was performed.Relevant literature regarding the application of cognitive reserve in poststroke cognitive impairment was retrieved from the Web of Science core collection database from January 2010 through January 2024.Citespace 6.3.R1(64-bit)was employed to visualize and analyze literature data,including general literature analysis,national publication distribution,literature co-citation,journal co-citation,keyword co-citation,keyword clustering,literature co-citation,and literature co-citation clustering.Results:A total of 860 articles were retrieved,indicating a rising trend in publications in this field,with the United States leading in publication count and FRONT NEUROL being the most frequently cited journal.The most frequently cited references usually focus on the prevention and influence factors of cognitive impairment and dementia.Conclusions:After eliminating keywords similar to the search terms,the top 3 keywords with the highest frequency and highest mediated centrality were dementia,cognitive influences,and risk factors,while education,influences,and cognitive assessment were emerging research focuses.展开更多
To the editor:Social communication impairment(SCI)is a core symptom of autism spectrum disorder(ASD),and evidence-based interventions targeting this domain remain limited.In the past decade,repetitive transcranial mag...To the editor:Social communication impairment(SCI)is a core symptom of autism spectrum disorder(ASD),and evidence-based interventions targeting this domain remain limited.In the past decade,repetitive transcranial magnetic stimulation(rTMS),one of the most commonly applied non-invasive neurostimulation techniques,has shown efficacy in treating neuropsychiatric disorders,such as depression.展开更多
BACKGROUND Mild behavioral impairment(MBI)refers to the neurobehavioral symptoms observed in older adults that may be potential risk factors for neurodegenerative diseases.While a significant number studies have explo...BACKGROUND Mild behavioral impairment(MBI)refers to the neurobehavioral symptoms observed in older adults that may be potential risk factors for neurodegenerative diseases.While a significant number studies have explored the association between cerebrospinal fluid and MBI,only a few have examined the connection between plasma biomarkers and MBI.AIM To examine the prevalence of MBI in healthy older adults(HOAs)and individuals with mild cognitive impairment(MCI),as well as the association between MBI and plasma biomarkers of Alzheimer’s disease(AD).METHODS We enrolled a total of 241 subjects,which included 136 HOAs and 105 MCIs,from the Yuhua District of Shijiazhuang City,Hebei Province,China.The MBI symp-tom checklist(MBI-C)was utilized for the assessment and diagnosis of MBI,and a score of MBI-C≥6.5 was considered indicative of the condition.Fasting venous blood samples were collected from 70 patients,32 HOAs and 38 MCIs,and levels of amyloidβ-protein(Aβ)40,Aβ42,and hyperphosphorylated tau(p-Tau217)in these samples were measured using an enzyme-linked immunosorbent assay.RESULTS The prevalence of MBI in the HOAs and MCI groups was 4.4%and 15.3%,respectively(χ^(2)=7.262,P=0.007),with particularly notable decreases in motivation and increases in impulse dyscontrol(the highest detection rate)and social inappropriateness(P<0.05).The total MBI score correlated with Aβ42 and p-Tau217(r=-0.385,P=0.019;r=-0.330,P=0.041),but not with Aβ40 or the Aβ42/40 ratio.Among the subdomains,impulse dyscontrol was correlated with Aβ42(r=-0.401,P=0.025).CONCLUSION Both MCI and HOAs have exhibited a higher prevalence of MBI,with changes in impulse control behavior being the most common.MBI not only presents as an independent risk factor for cognitive decline but is also linked with AD-related peripheral biomarkers.展开更多
文摘The intersection of visual impairment and mental health has profound effects on quality of life and warrants attention from healthcare providers,educators,and policymakers.With 20 million children under the age of 14 affected globally,older adults also experience significant psychological impact including depression,anxiety,and cognitive impairment.The implications of vision-related challenges extend far beyond mere sight.Depression and anxiety,exacerbated by social isolation and reduced physical activity,underscore the need for comprehensive interventions that address both medical and psychosocial dimensions.By recognizing the profound impact of ocular morbidities like strabismus,myopia,glaucoma,and age-related macular degeneration on mental health and investing in effective treatments and inclusive practices,society can pave the way for a healthier,more equitable future for affected individuals.There is evidence that myopic children experience a higher prevalence of depressive symptoms compared to their normal peers,and interventions like the correction of strabismus can enhance psychological outcome-demonstrating the value of an integrated management approach.
基金supported by the National Natural Science Foundation of China(81903416).
文摘Dementia is a growing global health burden,with mild cognitive impairment(MCI)serving as a critical transitional stage[1].Identifying the nutritional risk factors is crucial for prevention.While nutrition plays a key role in preventing age-related diseases and staple foods are a major dietary source,existing research on cognitive function has predominantly emphasized whole-grain consumption.There is limited evidence regarding the effects of specific staple food types on MCI.
基金supported by the Major Project of Wuxi Municipal Health Commission[grant number:Z202406]the Jiangsu Commission of Health Program[grant number:M2024010]+3 种基金the National Key Research and Development Program[grant number:2022YFC3600600]the China Ministry of Science and Technology grants[grant number:2009BAI77B03]the Shanghai Municipal Education Commission-Gaofeng Clinical Medicine Grant Support[grant number:20172029]the Innovative Research Team of High-level Local Universities in Shanghai[grant number:ZDCX20211201].
文摘Background As the population in China rapidly ages,the prevalence of mild cognitive impairment(MCI)is increasing considerably.However,the causes of MCI vary.The continued lack of understanding of the various subtypes of MCI impedes the implementation of effective measures to reduce the risk of advancing to more severe cognitive diseases.Aims To estimate the prevalence and incidence rates of two MCI subtypes—amnestic MCI(aMCI)and vascular cognitive impairment without dementia(VCIND)—and to determine modifiable factors for them among older individuals in a multiregional Chinese cohort.Method This 1-year longitudinal study surveyed a random sample of participants aged≥60 years from a large,community-dwelling cohort in China.Baseline lifestyle data were self-reported,while vascular and comorbid conditions were obtained from medical records and physical examinations.In total,3514 and 2051 individuals completed the baseline and 1-year follow-up assessments,respectively.Logistic and linear regression analyses were used to identify the modifiable factors for MCI subtypes and predictors of cognitive decline,respectively.Results Among our participants,aMCI and VCIND demonstrated prevalence of 14.83%and 2.71%,respectively,and annual incidence(per 1000 person-years)of 69.6 and 10.6,respectively.The risk factor for aMCI was age,whereas its protective factors were high education level,tea consumption and physical activity.Moreover,VCIND risk factors were age,hypertension and depression.The presence of endocrine disease,cerebral trauma or hypertension was associated with a faster decline in cognition over 1 year.Conclusions MCI is a serious health problem in China that will only worsen as the population ages if no widespread interventions are implemented.Preventive strategies that promote brain activity and support healthy lifestyle choices are required.We identified modifiable factors for MCI in older individuals.The easy-to-adopt solutions such as tea consumption and physical activity can aid in preventing MCI.
基金supported by Applied Basic Research Foundation of Yunnan Province,Nos.202301AS070045,202101AY070001-115(to XY and BL)National Natural Science Foundation of China,No.81960242(to XY)。
文摘Cognitive impairment is a particularly severe non-motor symptom of Parkinson's disease that significantly diminishes the quality of life of affected individuals.Identifying reliable biomarkers for cognitive impairment in Parkinson's disease is essential for early diagnosis,prognostic assessments,and the development of targeted therapies.This review aims to summarize recent advancements in biofluid biomarkers for cognitive impairment in Parkinson's disease,focusing on the detection of specific proteins,metabolites,and other biomarkers in blood,cerebrospinal fluid,and saliva.These biomarkers can shed light on the multifaceted etiology of cognitive impairment in Parkinson's disease,which includes protein misfolding,neurodegeneration,inflammation,and oxidative stress.The integration of biofluid biomarkers with neuroimaging and clinical data can facilitate the development of predictive models to enhance early diagnosis and monitor the progression of cognitive impairment in patients with Parkinson's disease.This comprehensive approach can improve the existing understanding of the mechanisms driving cognitive decline and support the development of targeted therapeutic strategies aimed at modifying the course of cognitive impairment in Parkinson's disease.Despite the promise of these biomarkers in characterizing the mechanisms underlying cognitive decline in Parkinson's disease,further research is necessary to validate their clinical utility and establish a standardized framework for early detection and monitoring of cognitive impairment in Parkinson's disease.
基金supported by Technological Innovation 2030-Major Projects of“Brain Science and Brain-like Research,”No.2022ZD0206200(to XG)the National Natural Science Foundation of China,No.82371245(to SJ),82102246(to XD),81701092(to XG)+2 种基金the Natural Science Foundation of Shandong Province,No.ZR2020MH129(to SJ)Shanghai Municipal Key Clinical Specialty,No.shslczdzk03601Shanghai Engineering Research Center of Peri-operative Organ Support and Function Preservation,No.20DZ2254200。
文摘Adult hippocampal neurogenesis is linked to memory formation in the adult brain,with new neurons in the hippocampus exhibiting greater plasticity during their immature stages compared to mature neurons.Abnormal adult hippocampal neurogenesis is closely associated with cognitive impairment in central nervous system diseases.Targeting and regulating adult hippocampal neurogenesis have been shown to improve cognitive deficits.This review aims to expand the current understanding and prospects of targeting neurogenesis in the treatment of cognitive impairment.Recent research indicates the presence of abnormalities in AHN in several diseases associated with cognitive impairment,including cerebrovascular diseases,Alzheimer's disease,aging-related conditions,and issues related to anesthesia and surgery.The role of these abnormalities in the cognitive deficits caused by these diseases has been widely recognized,and targeting AHN is considered a promising approach for treating cognitive impairment.However,the underlying mechanisms of this role are not yet fully understood,and the effectiveness of targeting abnormal adult hippocampal neurogenesis for treatment remains limited,with a need for further development of treatment methods and detection techniques.By reviewing recent studies,we classify the potential mechanisms of adult hippocampal neurogenesis abnormalities into four categories:immunity,energy metabolism,aging,and pathological states.In immunity-related mechanisms,abnormalities in meningeal,brain,and peripheral immunity can disrupt normal adult hippocampal neurogenesis.Lipid metabolism and mitochondrial function disorders are significant energy metabolism factors that lead to abnormal adult hippocampal neurogenesis.During aging,the inflammatory state of the neurogenic niche and the expression of aging-related microRNAs contribute to reduced adult hippocampal neurogenesis and cognitive impairment in older adult patients.Pathological states of the body and emotional disorders may also result in abnormal adult hippocampal neurogenesis.Among the current strategies used to enhance this form of neurogenesis,physical therapies such as exercise,transcutaneous electrical nerve stimulation,and enriched environments have proven effective.Dietary interventions,including energy intake restriction and nutrient optimization,have shown efficacy in both basic research and clinical trials.However,drug treatments,such as antidepressants and stem cell therapy,are primarily reported in basic research,with limited clinical application.The relationship between abnormal adult hippocampal neurogenesis and cognitive impairment has garnered widespread attention,and targeting the former may be an important strategy for treating the latter.However,the mechanisms underlying abnormal adult hippocampal neurogenesis remain unclear,and treatments are lacking.This highlights the need for greater focus on translating research findings into clinical practice.
基金supported by Postgraduate Research&Practice Innovation Program of Jiangsu Province,No.KYCX25_3785(to JY).
文摘Ischemic stroke has a higher survival rate and is more likely to result in cognitive impairment than hemorrhagic stroke.The primary pathological mechanism underlying cognitive impairment involves dysfunction of neural circuits and damage to specific brain regions.This review aims to investigate the role of the hippocampus in cognitive impairment following a stroke.A review of the literature suggests that the hippocampus is a metabolically active structure that is easily involved in various metabolic states,such as hypoxia and hypoglycaemia.The functional changes in hippocampal cells associated with poststroke cognitive impairment mainly manifest as neuronal apoptosis,impaired synaptic plasticity,and decreased neurogenesis.The primary pathological mechanism of poststroke cognitive impairment involves a complex cascade of reactions,including neuroinflammatory activation,bursts of oxidative stress,and neuronal apoptosis induced by mitochondrial dysfunction.Interventional drugs for cognitive impairment after cerebral ischemia include neuroprotective drugs,traditional Chinese medicines and their extracts,and stem cell therapies.Many of these drugs have unique advantages,including the inhibition of neuroinflammation,the prevention of apoptosis,and the promotion of neurogenesis.They hold great potential for the prevention and treatment of cognitive impairment following cerebral ischemia.However,most current studies are animal experiments,and relatively few clinical studies exist.In future research,emphasis should be placed on interventions for cognitive impairment following cerebral ischemia.These findings offer novel perspectives for the treatment of cognitive impairment after cerebral ischemia.Finally,the role of hippocampal cell dysfunction in other diseases associated with cognitive decline is briefly discussed.The aim of this review is to provide researchers with a comprehensive overview of the role of the hippocampus in cognitive impairment and its intervention strategies.
基金Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences,Grant/Award Number:2021-I2M-1-034Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences,Grant/Award Number:2023-PT180-01+1 种基金PUMC Innovation Fund for Graduate Students,Grant/Award Number:2017-1001-07National Natural Science Foundation of China,Grant/Award Number:82161138027。
文摘Background:The absence of effective animal models for sporadic Alzheimer's disease(AD)remains a pivotal barrier to therapy development.Because methanol metabolism produces endogenous formaldehyde,a neurotoxic agent linked to cognitive decline,this study investigated whether chronic,low-dose methanol exposure could recapitulate AD-like pathology and cognitive deficits in rhesus monkey,thereby establishing a nonhuman primate animal model driven by this environmental-metabolic insult.Methods:Adult rhesus monkeys received low-concentration methanol for 9 months.Behavioral tests for cognition,locomotion,sleep,and vision were conducted.Postmortem analyses involved histopathological examination,immunohistochemistry,immunofluorescence,and Western blot to evaluate neuronal integrity,microglial activation,and the expression of key proteins associated with AD(amyloid-β[Aβ],phosphorylated tau,TAR DNA-binding protein 43[TDP-43])and cellular stress(synaptic markers,mitochondrial fission,autophagy,and apoptosis-related proteins).Results:Chronic methanol exposure led to progressive cognitive and memory impairment without significant motor or visual deficits.Neuropathology revealed brain atrophy,neuronal loss,synaptic damage,microglial activation,and mitochondrial structural disorganization.Critically,the exposed animals exhibited hallmark AD-like molecular alterations,including increased Aβ deposition,tau hyperphosphorylation,and TDP-43 dysregulation.Furthermore,neurotoxicity was associated with elevated urinary formaldehyde,enhanced mitochondrial fission,increased autophagy,and elevated apoptosis.Conclusion:Chronic low-dose methanol exposure in rhesus monkeys recapitulates progressive cognitive deficits and AD-like neuropathological features.This model,driven by endogenous formaldehyde toxicity,effectively mimics key aspects of sporadic AD.Our findings shed light on the neurotoxic mechanisms of methanol and propose a reproducible and translationally relevant nonhuman primate model for studying AD pathogenesis and evaluating potential therapeutics.
文摘The increasing global prevalence of mild cognitive impairment(MCI)necessitates a paradigm shift in early detection strategies.Conventional neuropsychological assessment methods,predominantly paper-and-pencil tests such as the Mini-Mental State Examination and the Montreal Cognitive Assessment,exhibit inherent limitations with respect to accessibility,administration burden,and sensitivity to subtle cognitive decline,particularly among diverse populations.This commentary critically examines a recent study that champions a novel approach:The integration of gait and handwriting kinematic parameters analyzed via machine learning for MCI screening.The present study positions itself within the broader landscape of MCI detection,with a view to comparing its advantages against established neuropsychological batteries,advanced neuroimaging(e.g.,positron emission tomography,magnetic resonance imaging),and emerging fluid biomarkers(e.g.,cerebrospinal fluid,blood-based assays).While the study demonstrates promising accuracy(74.44%area under the curve 0.74 with gait and graphic handwriting)and addresses key unmet needs in accessibility and objectivity,we highlight its cross-sectional nature,limited sample diversity,and lack of dual-task assessment as areas for future refinement.This commentary posits that kinematic biomarkers offer a distinctive,scalable,and ecologically valid approach to widespread MCI screening,thereby complementing existing methods by providing real-world functional insights.Future research should prioritize longitudinal validation,expansion to diverse cohorts,integration with multimodal data including dual-tasking,and the development of highly portable,artificial intelligence-driven solutions to achieve the democratization of early MCI detection and enable timely interventions.
基金funded by Shanghai Baiyulan Pujiang Project(No.24PJD087)funded by the National Natural Science Foundation of China(No.12401347)+5 种基金Shanghai“Science and Technology Innovation Action Plan”Computational Biology Key Project(Nos.23JS1400500 and 23JS1400800)Chinese MOE Foundation on Humanities and Social Sciences(No.23YJC910006)the Natural Science Foundation of Shanghai(No.24ZR1420400)MWB was funded by NIH/NIA(Nos.R01AG082073,R01AG079280,and P30AG062429)HHF was funded by NIH/NIA(Nos.U19AG079774-01,R01AG061146,P30AG062429,R01AG076634-01,CIHR 137794)funded by NIH/NIA R01AG064002,P30AG062429,R01AG076634,and the Epstein Family Alzheimer’s Research Collaboration.
文摘Traditional clinical subtype classifications(such as amnestic and non-amnestic mild cognitive impairment)rely on subjective interpretations of overlapping patterns of performance on cognitive tests,which may lead to unreliable categorization.A more precise and objective classification of mild cognitive impairment subtypes can be achieved through data-driven clustering techniques.However,because previous studies have not restricted their cohorts to patients who have mild cognitive impairment with the pathology of Alzheimer’s disease,the nature of cognitive variability and its impact on disease progression in a strictly defined biomarker-positive preclinical Alzheimer’s disease cohort remains unknown.We examined cognitive heterogeneity among participants with mild cognitive impairment due to Alzheimer’s disease and evaluated its prognostic utility.Neuropsychological test data from 389 patients with mild cognitive impairment in whom the cerebrospinal fluid biomarker confirmed Alzheimer’s disease were obtained from the Alzheimer’s Disease Neuroimaging Initiative cohorts.Principal component analysis and model-based clustering were used to identify cognitive profiles,which were then validated through a 100-time bootstrap analysis.Pairwise comparisons tested for differences between the identified subgroups in participant characteristics,scores on cognitive and clinical outcomes,levels of cerebrospinal fluid biomarkers,and magnetic resonance imaging-derived brain volumes.Longitudinal analyses evaluated differences in rate of change of magnetic resonance imaging volumetric measurements and clinical outcomes over 48 months.Survival analysis assessed risk for conversion to dementia.Alpha-synuclein levels and white matter hyperintensity volumes were considered for sensitivity analysis.Two distinct cognitive profiles were identified:a“typical”group(56.04%of the sample)that demonstrated relatively poorer scores on memory testing than non-memory tests,and an“atypical”group(43.96%of the sample)with smaller differences between memory and non-memory measures,indicating a more uniform pattern of impairment across cognitive domains.While the groups had comparable levels of overall cognitive impairment and cerebrospinal fluid biomarkers of Alzheimer’s disease,the typical group displayed accelerated atrophy rates every 6 months across multiple brain regions(hippocampus:29.02 mm^(3),standard error[SE]=10.13,P=0.005;whole brain:1799.85 mm^(3),SE=781.57,P=0.023;entorhinal cortex:22.26 mm^(3),SE=11.15,P=0.048;fusiform gyrus:66.24 mm^(3),SE=28.53,P=0.021).Survival analysis revealed markedly higher dementia conversion risk(hazard ratio:1.70,95%confidence interval:1.27,2.27,P<0.001)and shorter progression time in the typical group.These findings persisted after controlling for comorbid pathologies.In conclusion,this data-driven approach identified two distinct cognitive subtypes of mild cognitive impairment due to Alzheimer’s disease that differed in their rates of clinical decline and neurodegeneration.These findings could be used to improve prognostic models and inform clinical trial stratification.
基金supported by Grants from the National Natural Science Foundation of China(82330041 and 82201326)the China Postdoctoral Research Foundation(GZC20230898)the Science and Technology Innovation Team Project to Xiaochuan Wang from the Department of Science and Technology of Hubei Province(2022-72-18).
文摘Sepsis-associated encephalopathy(SAE)is a severe neurological syndrome marked by widespread brain dysfunctions due to sepsis,yet the underlying mechanisms remain elusive.The current study,using a Lipopolysaccharide(LPS)-induced septic rat model,revealed the hyperphosphorylation of tau and cognitive impairments,accompanied by the release of inflammatory cytokines and activation of glial cells in the hippocampal dentate gyrus region of septic rats.Proteomic and bioinformatic analyses identified C-X-C motif chemokine ligand 10(CXCL10)as a central regulator of neuroinflammation.LPS triggered CXCL10 secretion in astrocytes,and astrocyte-conditioned medium from LPS-treated astrocytes induced tau hyperphosphorylation and synaptic deficits.Recombinant CXCL10 recapitulated these effects in vitro and in vivo.Blocking CXCL10–CXCR3 interaction reversed tau phosphorylation,synaptic impairment,and cognitive decline.Mechanistically,CXCL10–CXCR3 interaction activated CaMKII,driving tau hyperphosphorylation,while CaMKII inhibition restored synaptic protein levels.These findings establish CXCL10 as a key driver of tau pathology in SAE and suggest CXCL10–CXCR3 as a therapeutic target for sepsis-induced cognitive impairments.
文摘Purpose: Individuals with mild cognitive impairment (MCI) frequently experience negative emotions, which are closely correlated with an accelerated rate of cognitive decline and the subsequent transition to a state of dementia. Despite networked cognitive training has been demonstrated to enhance cognitive function in MCI, its effectiveness for negative emotions is still unknown. This review aimed to exam the influences of networked cognitive training on negative emotions and quality of life in people with MCI. Methods: Searches for eligible studies were conducted using PubMed, Web of Science, EMBASE, Cochrane Library, Psyc INFO, CNKI, Wanfang database, VIP database, and Sinomed. The retrieval time limit was set from their inception to 17 December 2025. The articles were reviewed and extracted by two researchers, and their quality was evaluated using the Cochrane risk-of-bias assessment tool. Subsequently, a meta-analysis was carried out utilizing RevMan 5.4 software. Results: The review comprised 13 randomized controlled trials with 626 individuals. The meta-analysis demonstrated that networked cognitive training significantly improved depression (SMD = -0.36;95% CI [-0.73, -0.00];p = .050), anxiety (SMD = -0.32;95% CI [-0.57, -0.06];p < .050), and quality of life (MD = 2.54;95% CI [0.98, 4.10];p < .001). In terms of the comparison of apathy, the effect of intervention was unclear. Conclusions: From these meta-analysis results, networked cognitive training may help patients for MCI with their anxiety, depression, and overall quality of life. However, because there are so few randomized controlled trials available, the evidence regarding apathy is still ambiguous. More thorough randomized controlled trials with larger samples are necessary to verify the significance of networked cognitive training on apathy and to consolidate the findings.
基金supported by the Science Research Start-up Fund for Doctor of Shanxi Medical University,No.SD2114(to JL).
文摘Cognitive impairment is a complex neurodegenerative disorder,and increased homocysteine levels are recognized as a major risk factor for this condition.Epigenetic modifications,particularly histone acetylation,have been implicated in the progression of cognitive impairment;however,the mechanisms underlying hyperhomocysteinemia-induced cognitive impairment remain unclear.In this study,we developed an hyperhomocysteinemia-induced cognitive impairment model by feeding mice a high-methionine diet and conducted behavioral and molecular analyses to elucidate the mechanisms involved in cognitive impairment.Behavioral experiments revealed significant cognitive deficits and neuroinflammation accompanied by a marked decrease in histone H3 lysine 27 acetylation in the hippocampus and cortex.Furthermore,metabolomic profiling and chromatin immunoprecipitation sequencing demonstrated substantial shifts in the levels of homocysteine metabolites and identified histone H3 lysine 27 acetylation-targeted genes involved in synaptic long-term potentiation,including Gria1,Gria3,Grin2a,Grin2b,Slc1a1,Slc24a2,Ptk2b,and Src.RNA sequencing confirmed that hyperhomocysteinemia induced neurodegeneration.In vitro experiments confirmed that decreased histone H3 lysine 27 acetylation downregulates the expression of these target genes in homocysteine-treated HT-22 cells,thereby impairing synaptic plasticity.Collectively,these findings suggest that aberrant expression of long-term potentiation-related genes regulated by histone H3 lysine 27 acetylation is a key driver of hyperhomocysteinemia-induced cognitive impairment.Targeting histone H3 lysine 27 acetylation-mediated epigenetic dysregulation may be a promising therapeutic strategy,offering potential avenues for intervention in individuals with cognitive impairment and neurodegenerative disorders.
文摘With the intensification of population aging in China,the problem of cognitive impairment in the elderly has become increasingly prominent,attracting widespread attention from all sectors of society.Geriatric cognitive impairment is characterized by chronicity,which not only seriously threatens the health of the elderly and reduces their quality of life,but also imposes a heavy burden on families and society due to its long course.Attaching importance to and strengthening the chronic disease management of elderly cognitive impairment has profound significance for delaying disease progression,improving patients’quality of life,and reducing the burden of family care.Therefore,this paper first comprehensively understands elderly cognitive impairment by briefly elaborating on its definition and characteristics;on this basis,it focuses on exploring effective strategies for the chronic disease management of elderly cognitive impairment,hoping to provide new ideas and methods for the management of this condition and offer useful references for relevant clinical research and practice.
基金supported by the National Natural Science Foundation of China(32172210)the Shandong Provincial Natural Science Foundation(ZR2025QC295).
文摘Neurodegenerative diseases,such as Alzheimer’s disease and Parkinson’s disease,are associated with cognitive impairment and impaired brain glucose metabolism,posing significant challenges for the public health.We previously demonstrated that cyanidin 3-O-β-galactoside(Cy3Gal)from black chokeberry alleviated cognitive impairment in aging mice through regulating brain energy metabolism in a direct way.However,the indirect mechanisms in mitigating brain glucose hypometabolism remain underexplored.Here,we utilized a bilaterally intracerebroventricular injection of streptozotocin(ICV/STZ,3 mg/kg bw)-induced brain glucose hypometabolism model to investigate the effects of Cy3Gal on cognitive impairment alleviation.Our findings revealed that Cy3Gal administration significantly improved memory deficit and cognitive impairment in ICV/STZ-administrated mice.Subsequently,Cy3Gal showed excellent abilities in inhibiting astrocyte overactivation,regulating neurotransmitters metabolism,and promoting synaptic plasticity.Furthermore,Cy3Gal enhanced brain glucose metabolism by improving glycolysis and the TCA cycle.Additionally,Cy3Gal modulated levels of gut microbiota-derived metabolites,including acetate,butyrate,histidine,glutamine,serine,valine and isoleucine,which were closely linked to brain glucose metabolism.The in vitro results further demonstrated that these metabolites played an important role in the neuron-astrocyte energy metabolism,which accounted for the alleviation of glucose hypometabolism.Overall,our findings suggest that Cy3Gal mitigates ICV/STZ-induced cognitive impairment by modulating gut microbiota-derived short-chain fatty acids and amino acids,which in turn improves brain glucose metabolism.
基金Supported by National Natural Science Foundation of China-funded Project:Study on Mechanism of“Smoothing The Liver Therapy”on Working Memory of the Patients with Mild Cognitive Impairment Caused by Negative Emotion Regulation(No.81473556)Effects and Mechanism of Liver’s Failing to Facilitate the Coursing of Qi on Decline Process of Cognitive Function of Normal People and Patients with MCI(No.81873208)。
文摘OBJECTIVE:To examine the differences in cognitive processing between patients with mild cognitive impairment(MCI)of different Traditional Chinese Medicine(TCM)syndrome types to provide evidence supporting the TCM typing of MCI.METHODS:Participants were screened using a battery of scales for spleen and kidney deficiency(SKD)/liver Qi stagnation(LQS)-type MCI or those without syndrome or normal control(NC).Following sex,age,and educational matching,behavioral and electroencephalographic data were recorded using the verbal N-back experimental paradigm.The data were then analyzed and compared with respect to the reaction time and correctness of the participants in each group,as well as the amplitude and latency of the event-related potential(ERP)components of P2,N2,and P3.RESULTS:There were no statistically significant differences in the accuracy or reaction times of the behavioral data of the groups.Regarding ERP data,the SKD group had a shorter P2 latency than the LQS and NC groups,while the latter two groups did not differ statistically.The SKD group had a shorter N2 latency than the NC group,while the SKD group did not differ from the LQS group.The SKD and LQS groups had a shorter P3 latency than the NC group.CONCLUSION:Our study offers objective evidence of the distinction between the types of TCM syndrome.Different types of TCM syndromes produce different disease mechanisms,resulting in brain damage with different presentations of cognitive impairment and cognitive processing characteristics.
基金supported by the Beijing Nova Program,Nos.20230484436,Z211100002121038the Chinese Institutes for Medical Research,No.CX23YQ01+1 种基金the NationalNatural Science Foundation of China,Nos.32100925,82027802Beijing-Tianjin-Hebei Basic Research Cooperation Project,No.22JCZXJC00190(all to XJand JL).
文摘Vascular cognitive impairment and dementia is a debilitating neurological disorder caused by chronic cerebral hypoperfusion,for which no effective causative treatments are currently available.Intermittent hypoxia has been shown to enhance cerebral blood flow in mice,but its efficacy in a model of vascular cognitive impairment and dementia remains unclear.In this study,we established a mouse model of vascular cognitive impairment and dementia by bilateral carotid artery stenosis.Intermittent hypoxia was induced before and after this stenosis.We found that intermittent hypoxia increased cerebral blood flow,oxygen saturation,and microcirculation in the prefrontal cortex and hippocampus in the model mice,without causing neurovascular damage.Additionally,intermittent hypoxia significantly improved cognitive function in the mouse model of vascular cognitive impairment and dementia,with perconditioning showing greater efficacy than preconditioning.Improvements in cerebral microcirculation and blood flow were positively correlated with cognitive recovery.Even in a mouse model of vascular cognitive impairment and dementia with comorbidities induced by a high-fat,high-fructose diet,intermittent hypoxic perconditioning demonstrated protective effects on cognitive function.Proteomic analysis indicated that mitochondrial protection is a key mechanism,particularly through upregulating NDUFB8 expression and increasing the activity of mitochondrial complex I.These findings suggest that intermittent hypoxia is a potential non-invasive strategy for the prevention and treatment of vascular cognitive impairment and dementia.
文摘According to the Japanese Ministry of Health,Labour,and Welfare,14.2%of people were aged>75 years in Japan in 2018,and this number continues to rise.With population aging,the incidence of congestive heart failure(CHF)is also increasing.[1–3]Reports have shown that the presence of cognitive impairment(CI)in patients with CHF is associated with poor prognosis,[4–6]and the degree of CI is related to CHF severity.
基金supported by the Scientific Research Foundation of Hunan Provincial Education Department(No.23B0517)the National Natural Science Foundation of China(No.82360665).
文摘Objective:To examine the research trends and hotspots of the application of cognitive reserve in stroke cognitive impairment using CiteSpace and provide a reference for developing effective measures to reduce the incidence of cognitive impairment in these patients.Methods:Using CiteSpace software,a visual analysis of 860 included articles related to cognitive reserve in stroke cognitive impairment patients was performed.Relevant literature regarding the application of cognitive reserve in poststroke cognitive impairment was retrieved from the Web of Science core collection database from January 2010 through January 2024.Citespace 6.3.R1(64-bit)was employed to visualize and analyze literature data,including general literature analysis,national publication distribution,literature co-citation,journal co-citation,keyword co-citation,keyword clustering,literature co-citation,and literature co-citation clustering.Results:A total of 860 articles were retrieved,indicating a rising trend in publications in this field,with the United States leading in publication count and FRONT NEUROL being the most frequently cited journal.The most frequently cited references usually focus on the prevention and influence factors of cognitive impairment and dementia.Conclusions:After eliminating keywords similar to the search terms,the top 3 keywords with the highest frequency and highest mediated centrality were dementia,cognitive influences,and risk factors,while education,influences,and cognitive assessment were emerging research focuses.
基金supported by grants from the National Natural Science Foundation of China(82125032,81930095,82204048 and 81761128035)the Science and Technology Commission of Shanghai Municipality(19410713500 and 2018SHZDZX01)+3 种基金the Foundation of Shanghai Municipal Commission of Health and Family Planning(GWV-10.1-XK07,2020CXJQ01 and 2018YJRC03)the Shanghai Clinical Key Subject Construction Project(shslczdzk02902)the Innovative Research Team of High-Level Local Universities in Shanghai(SHSMU-ZDCX20211100)the Guangdong Key Project(2018B030335001).
文摘To the editor:Social communication impairment(SCI)is a core symptom of autism spectrum disorder(ASD),and evidence-based interventions targeting this domain remain limited.In the past decade,repetitive transcranial magnetic stimulation(rTMS),one of the most commonly applied non-invasive neurostimulation techniques,has shown efficacy in treating neuropsychiatric disorders,such as depression.
基金Supported by the Government Funded Clinical Medicine Excellent Talents Training Project of Hebei Province,No.ZF2024136National Science Foundation of Hebei Province,No.H2022206544Science and Technology Program of Hebei Province,No.SG2021189。
文摘BACKGROUND Mild behavioral impairment(MBI)refers to the neurobehavioral symptoms observed in older adults that may be potential risk factors for neurodegenerative diseases.While a significant number studies have explored the association between cerebrospinal fluid and MBI,only a few have examined the connection between plasma biomarkers and MBI.AIM To examine the prevalence of MBI in healthy older adults(HOAs)and individuals with mild cognitive impairment(MCI),as well as the association between MBI and plasma biomarkers of Alzheimer’s disease(AD).METHODS We enrolled a total of 241 subjects,which included 136 HOAs and 105 MCIs,from the Yuhua District of Shijiazhuang City,Hebei Province,China.The MBI symp-tom checklist(MBI-C)was utilized for the assessment and diagnosis of MBI,and a score of MBI-C≥6.5 was considered indicative of the condition.Fasting venous blood samples were collected from 70 patients,32 HOAs and 38 MCIs,and levels of amyloidβ-protein(Aβ)40,Aβ42,and hyperphosphorylated tau(p-Tau217)in these samples were measured using an enzyme-linked immunosorbent assay.RESULTS The prevalence of MBI in the HOAs and MCI groups was 4.4%and 15.3%,respectively(χ^(2)=7.262,P=0.007),with particularly notable decreases in motivation and increases in impulse dyscontrol(the highest detection rate)and social inappropriateness(P<0.05).The total MBI score correlated with Aβ42 and p-Tau217(r=-0.385,P=0.019;r=-0.330,P=0.041),but not with Aβ40 or the Aβ42/40 ratio.Among the subdomains,impulse dyscontrol was correlated with Aβ42(r=-0.401,P=0.025).CONCLUSION Both MCI and HOAs have exhibited a higher prevalence of MBI,with changes in impulse control behavior being the most common.MBI not only presents as an independent risk factor for cognitive decline but is also linked with AD-related peripheral biomarkers.
