The concept of the brain cognitive reserve is derived from the well-acknowledged notion that the degree of brain damage does not always match the severity of clinical symptoms and neurological/cognitive outcomes.It ha...The concept of the brain cognitive reserve is derived from the well-acknowledged notion that the degree of brain damage does not always match the severity of clinical symptoms and neurological/cognitive outcomes.It has been suggested that the size of the brain(brain reserve) and the extent of neural connections acquired through life(neural reserve) set a threshold beyond which noticeable impairments occur.In contrast,cognitive reserve refers to the brain's ability to adapt and reo rganize stru cturally and functionally to resist damage and maintain function,including neural reserve and brain maintenance,resilience,and compensation(Verkhratsky and Zorec,2024).展开更多
Challenges in the prevention and treatment of mild cognitive impairment associated with Alzheimer's disease:Increased life expectancy due to advancements in medical care has given rise to an aging population,accom...Challenges in the prevention and treatment of mild cognitive impairment associated with Alzheimer's disease:Increased life expectancy due to advancements in medical care has given rise to an aging population,accompanied by a surge in the incidence of incurable neurodegenerative diseases(NDDs).These diseases primarily affect the cognitive and behavioral functions of older adults by impacting brain activity.Mild cognitive impairment(MCI)is a neurodegenerative condition that affects a significant portion of the population.展开更多
Neuromodulation techniques effectively intervene in cognitive function,holding considerable scientific and practical value in fields such as aerospace,medicine,life sciences,and brain research.These techniques utilize...Neuromodulation techniques effectively intervene in cognitive function,holding considerable scientific and practical value in fields such as aerospace,medicine,life sciences,and brain research.These techniques utilize electrical stimulation to directly or indirectly target specific brain regions,modulating neural activity and influencing broader brain networks,thereby regulating cognitive function.Regulating cognitive function involves an understanding of aspects such as perception,learning and memory,attention,spatial cognition,and physical function.To enhance the application of cognitive regulation in the general population,this paper reviews recent publications from the Web of Science to assess the advancements and challenges of invasive and non-invasive stimulation methods in modulating cognitive functions.This review covers various neuromodulation techniques for cognitive intervention,including deep brain stimulation,vagus nerve stimulation,and invasive methods using microelectrode arrays.The non-invasive techniques discussed include transcranial magnetic stimulation,transcranial direct current stimulation,transcranial alternating current stimulation,transcutaneous electrical acupoint stimulation,and time interference stimulation for activating deep targets.Invasive stimulation methods,which are ideal for studying the pathogenesis of neurological diseases,tend to cause greater trauma and have been less researched in the context of cognitive function regulation.Non-invasive methods,particularly newer transcranial stimulation techniques,are gentler and more appropriate for regulating cognitive functions in the general population.These include transcutaneous acupoint electrical stimulation using acupoints and time interference methods for activating deep targets.This paper also discusses current technical challenges and potential future breakthroughs in neuromodulation technology.It is recommended that neuromodulation techniques be combined with neural detection methods to better assess their effects and improve the accuracy of non-invasive neuromodulation.Additionally,researching closed-loop feedback neuromodulation methods is identified as a promising direction for future development.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
Complex genetic relationships between neurodegenerative disorders and neuropsychiatric symptoms have been shown, suggesting shared pathogenic mechanisms and emphasizing the potential for developing common therapeutic ...Complex genetic relationships between neurodegenerative disorders and neuropsychiatric symptoms have been shown, suggesting shared pathogenic mechanisms and emphasizing the potential for developing common therapeutic targets. Apolipoprotein E(APOE) genotypes and their corresponding protein(Apo E) isoforms may influence the biophysical properties of the cell membrane lipid bilayer. However, the role of APOE in central nervous system pathophysiology extended beyond its lipid transport function. In the present review article, we analyzed the links existing between APOE genotypes and the neurobiology of neuropsychiatric symptoms in neurodegenerative and vascular diseases. APOE genotypes(APOE ε2, APOE ε3, and APOE ε4) were implicated in common mechanisms underlying a wide spectrum of neurodegenerative diseases, including sporadic Alzheimer's disease, synucleinopathies such as Parkinson's disease and Lewy body disease, stroke, and traumatic brain injury. These shared pathways often involved neuroinflammation, abnormal protein accumulation, or responses to acute detrimental events. Across these conditions, APOE variants are believed to contribute to the modulation of inflammatory responses, the regulation of amyloid and tau pathology, as well as the clearance of proteins such as α-synuclein. The bidirectional interactions among Apo E, amyloid and mitochondrial metabolism, immunomodulatory effects, neuronal repair, and remodeling underscored the complexity of Apo E's role in neuropsychiatric symptoms associated with these conditions since from early phases of cognitive impairment such as mild cognitive impairment and mild behavioral impairment. Besides Apo E-specific isoforms' link to increased neuropsychiatric symptoms in Alzheimer's disease(depression, psychosis, aberrant motor behaviors, and anxiety, not apathy), the APOE ε4 genotype was also considered a significant genetic risk factor for Lewy body disease and its worse cognitive outcomes. Conversely, the APOE ε2 variant has been observed not to exert a protective effect equally in all neurodegenerative diseases. Specifically, in Lewy body disease, this variant may delay disease onset, paralleling its protective role in Alzheimer's disease, although its role in frontotemporal dementia is uncertain. The APOE ε4 genotype has been associated with adverse cognitive outcomes across other various neurodegenerative conditions. In Parkinson's disease, the APOE ε4 allele significantly impacted cognitive performance, increasing the risk of developing dementia, even in cases of pure synucleinopathies with minimal co-pathology from Alzheimer's disease. Similarly, in traumatic brain injury, recovery rates varied, with APOE ε4 carriers demonstrating a greater risk of poor long-term cognitive outcomes and elevated levels of neuropsychiatric symptoms. Furthermore, APOE ε4 influenced the age of onset and severity of stroke, as well as the likelihood of developing stroke-associated dementia, potentially due to its role in compromising endothelial integrity and promoting blood–brain barrier dysfunction.展开更多
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 alterati...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.展开更多
BACKGROUND Cognitive frailty and depression are prevalent among the elderly,significantly impairing physical and cognitive functions,psychological well-being,and quality of life.Effective interventions are essential t...BACKGROUND Cognitive frailty and depression are prevalent among the elderly,significantly impairing physical and cognitive functions,psychological well-being,and quality of life.Effective interventions are essential to mitigate these adverse effects and enhance overall health outcomes in this population.AIM To evaluate the effects of exercise-cognitive dual-task training on frailty,cognitive function,psychological status,and quality of life in elderly patients with cognitive frailty and depression.METHODS A retrospective study was conducted on 130 patients with cognitive frailty and depression admitted between December 2021 and December 2023.Patients were divided into a control group receiving routine intervention and an observation group undergoing exercise-cognitive dual-task training in addition to routine care.Frailty,cognitive function,balance and gait,psychological status,and quality of life were assessed before and after the intervention.RESULTS After the intervention,the frailty score of the observation group was(5.32±0.69),lower than that of the control group(5.71±0.55).The Montreal cognitive assessment basic scale score in the observation group was(24.06±0.99),higher than the control group(23.43±1.40).The performance oriented mobility assessment score in the observation group was(21.81±1.24),higher than the control group(21.15±1.26).The self-efficacy in the observation group was(28.27±2.66),higher than the control group(30.05±2.66).The anxiety score in the hospital anxiety and depression scale(HADS)for the observation group was(5.86±0.68),lower than the control group(6.21±0.64).The depression score in the HADS for the observation group was(5.67±0.75),lower than the control group(6.27±0.92).Additionally,the scores for each dimension of the 36-item short form survey in the observation group were higher than those in the control group,with statistically significant differences(P<0.05).CONCLUSION Exercise-cognitive dual-task training is beneficial for improving frailty,enhancing cognitive function,and improving psychological status and quality of life in elderly patients with cognitive frailty and depression.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
A reduction in adult neurogenesis is associated with behavioral abnormalities in patients with Alzheimer's disease.Consequently,enhancing adult neurogenesis represents a promising therapeutic approach for mitigati...A reduction in adult neurogenesis is associated with behavioral abnormalities in patients with Alzheimer's disease.Consequently,enhancing adult neurogenesis represents a promising therapeutic approach for mitigating disease symptoms and progression.Nonetheless,nonpharmacological interventions aimed at inducing adult neurogenesis are currently limited.Although individual non-pharmacological interventions,such as aerobic exercise,acousto-optic stimulation,and olfactory stimulation,have shown limited capacity to improve neurogenesis and cognitive function in patients with Alzheimer's disease,the therapeutic effect of a strategy that combines these interventions has not been fully explored.In this study,we observed an age-dependent decrease in adult neurogenesis and a concurrent increase in amyloid-beta accumulation in the hippocampus of amyloid precursor protein/presenilin 1 mice aged 2-8 months.Amyloid deposition became evident at 4 months,while neurogenesis declined by 6 months,further deteriorating as the disease progressed.However,following a 4-week multifactor stimulation protocol,which encompassed treadmill running(46 min/d,10 m/min,6 days per week),40 Hz acousto-optic stimulation(1 hour/day,6 days/week),and olfactory stimulation(1 hour/day,6 days/week),we found a significant increase in the number of newborn cells(5'-bromo-2'-deoxyuridine-positive cells),immature neurons(doublecortin-positive cells),newborn immature neurons(5'-bromo-2'-deoxyuridine-positive/doublecortin-positive cells),and newborn astrocytes(5'-bromo-2'-deoxyuridine-positive/glial fibrillary acidic protein-positive cells).Additionally,the amyloid-beta load in the hippocampus decreased.These findings suggest that multifactor stimulation can enhance adult hippocampal neurogenesis and mitigate amyloid-beta neuropathology in amyloid precursor protein/presenilin 1 mice.Furthermore,cognitive abilities were improved,and depressive symptoms were alleviated in amyloid precursor protein/presenilin 1 mice following multifactor stimulation,as evidenced by Morris water maze,novel object recognition,forced swimming test,and tail suspension test results.Notably,the efficacy of multifactor stimulation in consolidating immature neurons persisted for at least 2weeks after treatment cessation.At the molecular level,multifactor stimulation upregulated the expression of neuron-related proteins(NeuN,doublecortin,postsynaptic density protein-95,and synaptophysin),anti-apoptosis-related proteins(Bcl-2 and PARP),and an autophagyassociated protein(LC3B),while decreasing the expression of apoptosis-related proteins(BAX and caspase-9),in the hippocampus of amyloid precursor protein/presenilin 1 mice.These observations might be attributable to both the brain-derived neurotrophic factor-mediated signaling pathway and antioxidant pathways.Furthermore,serum metabolomics analysis indicated that multifactor stimulation regulated differentially expressed metabolites associated with cell apoptosis,oxidative damage,and cognition.Collectively,these findings suggest that multifactor stimulation is a novel non-invasive approach for the prevention and treatment of Alzheimer's disease.展开更多
Cognitive bias,stemming from electronic measurement error and variability in human perception,exists in cognitive electronic warfare and affects the outcomes of conflicts.In this paper,the dynamic game approach is emp...Cognitive bias,stemming from electronic measurement error and variability in human perception,exists in cognitive electronic warfare and affects the outcomes of conflicts.In this paper,the dynamic game approach is employed to develop a model for cognitive bias induced by incomplete information and measurement errors in cognitive radar countermeasures.The payoffs for both parties are calculated using the radar's anti-jamming strategy matrix A and the jammer's jamming strategy matrix B.With perfect Bayesian equilibrium,a dynamic radar countermeasure model is established,and the impact of cognitive bias is analyzed.Drawing inspiration from the cognitive bias analysis method used in stock market trading,a cognitive bias model for cognitive radar countermeasures is introduced,and its correctness is mathematically proved.A gaming scenario involving the AN/SPY-1 radar and a smart jammer is set up to analyze the influence of cognitive bias on game outcomes.Simulation results validate the effectiveness of the proposed method.展开更多
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...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.展开更多
BACKGROUND Mild cognitive impairment(MCI)has a high risk of progression to Alzheimer’s disease.The disease is often accompanied by sleep disorders,and whether sleep disorders have an effect on brain function in patie...BACKGROUND Mild cognitive impairment(MCI)has a high risk of progression to Alzheimer’s disease.The disease is often accompanied by sleep disorders,and whether sleep disorders have an effect on brain function in patients with MCI is unclear.AIM To explore the near-infrared brain function characteristics of MCI with sleep disorders.METHODS A total of 120 patients with MCI(MCI group)and 50 healthy subjects(control group)were selected.All subjects underwent the functional near-infrared spec-troscopy test.Collect baseline data,Mini-Mental State Examination,Montreal Cognitive Assessment scale,fatigue severity scale(FSS)score,sleep parameter,and oxyhemoglobin(Oxy-Hb)concentration and peak time of functional near-infrared spectroscopy test during the task period.The relationship between Oxy-RESULTS Compared with the control group,the FSS score of the MCI group was higher(t=11.310),and the scores of Pittsburgh sleep quality index,sleep time,sleep efficiency,nocturnal sleep disturbance,and daytime dysfunction were higher(Z=-10.518,-10.368,-9.035,-10.661,-10.088).Subjective sleep quality and total sleep time scores were lower(Z=-11.592,-9.924).The sleep efficiency of the MCI group was lower,and the awakening frequency,rem sleep latency period,total sleep time,and oxygen desaturation index were higher(t=5.969,5.829,2.887,3.003,5.937).The Oxy-Hb concentration at T0,T1,and T2 in the MCI group was lower(t=14.940,11.280,5.721),and the peak time was higher(t=18.800,13.350,9.827).In MCI patients,the concentration of Oxy-Hb during T0 was negatively correlated with the scores of Pittsburgh sleep quality index,sleep time,total sleep time,and sleep efficiency(r=-0.611,-0.388,-0.563,-0.356).It was positively correlated with sleep efficiency and total sleep time(r=0.754,0.650),and negatively correlated with oxygen desaturation index(r=-0.561)and FSS score(r=-0.526).All comparisons were P<0.05.CONCLUSION Patients with MCI and sleep disorders have lower near-infrared brain function than normal people,which is related to sleep quality.Clinically,a comprehensive assessment of the near-infrared brain function of patients should be carried out to guide targeted treatment and improve curative effect.展开更多
Previous studies have shown that the compound(E)-2-(3,4-dihydroxystyryl)-3-hydroxy-4H-pyran-4-one(D30),a pyromeconic acid derivative,possesses antioxidant and anti-inflammatory properties,inhibits amyloid-β aggregati...Previous studies have shown that the compound(E)-2-(3,4-dihydroxystyryl)-3-hydroxy-4H-pyran-4-one(D30),a pyromeconic acid derivative,possesses antioxidant and anti-inflammatory properties,inhibits amyloid-β aggregation,and alleviates scopolamine-induced cognitive impairment,similar to the phase Ⅲ clinical drug resveratrol.In this study,we established a mouse model of Alzheimer's disease via intracerebroventricular injection of fibrillar amyloid-β to investigate the effect of D30 on fibrillar amyloid-β-induced neuropathology.Our results showed that D30 alleviated fibrillar amyloid-β-induced cognitive impairment,promoted fibrillar amyloid-β clearance from the hippocampus and cortex,suppressed oxidative stress,and inhibited activation of microglia and astrocytes.D30 also reversed the fibrillar amyloid-β-induced loss of dendritic spines and synaptic protein expression.Notably,we demonstrated that exogenous fibrillar amyloid-βintroduced by intracerebroventricular injection greatly increased galectin-3 expression levels in the brain,and this increase was blocked by D30.Considering the role of D30 in clearing amyloid-β,inhibiting neuroinflammation,protecting synapses,and improving cognition,this study highlights the potential of galectin-3 as a promising treatment target for patients with Alzheimer's disease.展开更多
This manuscript explores the recent study by Cui et al which assessed the interplay between inflammatory cytokines and brain-derived neurotrophic factor(BDNF)levels in first-episode schizophrenia patients.The study re...This manuscript explores the recent study by Cui et al which assessed the interplay between inflammatory cytokines and brain-derived neurotrophic factor(BDNF)levels in first-episode schizophrenia patients.The study revealed that higher levels of interleukin-6 and tumor necrosis factor-αcorrelated with reduced BDNF levels and poorer cognitive performance.Schizophrenia is a severe psy-chiatric disorder impacting approximately 1%of the global population,charac-terized by positive symptoms(hallucinations and delusions),negative symptoms(diminished motivation and cognitive impairments)and disorganized thoughts and behaviors.Emerging research highlights the role of BDNF as a potential biomarker for early diagnosis and therapeutic targeting.The findings from Cui et al’s study suggest that targeting neuroinflammation and enhancing BDNF levels may improve cognitive outcomes.Effective treatment approaches involve a com-bination of pharmacological and non-pharmacological interventions tailored to individual patient needs.Hence,monitoring cognitive and neuroinflammatory markers is essential for improving patient outcomes and quality of life.Conse-quently,this manuscript highlights the need for an integrated approach to schizo-phrenia management,considering both clinical symptoms and underlying neuro-biological changes.展开更多
The rapid advancement of Artificial Intelligence(AI)and Large Language Models(LLMs)has led to their increasing integration into various domains,from text generation and translation to question-answering.However,a crit...The rapid advancement of Artificial Intelligence(AI)and Large Language Models(LLMs)has led to their increasing integration into various domains,from text generation and translation to question-answering.However,a critical question remains:do these sophisticated models,much like humans,exhibit susceptibility to cognitive biases?Understanding the presence and nature of such biases in AI is paramount for assessing their reliability,enhancing their performance,and predicting their societal impact.This research specifically investigates the susceptibility of Google’s Gemini 1.5 Pro and DeepSeek,two prominent LLMs,to framing effects and confirmation bias.The study meticulously designed a series of experimental trials,systematically manipulating information proportions and presentation orders to evaluate these biases.In the framing effect experiment,a genetic testing decision-making scenario was constructed.The proportion of positive and negative information(e.g.,20%,50%,or 80%positive)and their presentation order were varied.The models’inclination towards undergoing genetic testing was recorded.For the confirmation bias experiment,two reports-one positive and one negative-about“RoboTaxi”autonomous vehicles were provided.The proportion of erroneous information within these reports(10%,30%,and 50%)and their presentation order were systematically altered,and the models’support for each report was assessed.The findings demonstrate that both Gemini 1.5 Pro and DeepSeek are susceptible to framing effects.In the genetic testing scenario,their decision-making was primarily influenced by the proportion of positive and negative information presented.When the proportion of positive information was higher,both models showed a greater inclination to recommend or proceed with genetic testing.Conversely,a higher proportion of negative information led to greater caution or a tendency not to recommend the testing.Importantly,the order in which this information was presented did not significantly influence their decisions in the framing effect scenarios.Regarding confirmation bias,the two models exhibited distinct behaviors.Gemini 1.5 Pro did not show an overall preference for either positive or negative reports.However,its judgments were significantly influenced by the order of information presentation,demonstrating a“recency effect,”meaning it tended to support the report presented later.The proportion of erroneous information within the reports had no significant impact on Gemini 1.5 Pro’s decisions.In contrast,DeepSeek exhibited an overall confirmation bias,showing a clear preference for positive reports.Similar to Gemini 1.5 Pro,DeepSeek’s decisions were also significantly affected by the order of information presentation,while the proportion of misinformation had no significant effect.These results reveal human-like cognitive vulnerabilities in advanced LLMs,highlighting critical challenges to their reliability and objectivity in decision-making processes.Gemini 1.5 Pro’s sensitivity to presentation order and DeepSeek’s general preference for positive information,coupled with its sensitivity to order,underscore the need for careful evaluation of potential cognitive biases during the development and application of AI.The study suggests that effective measures are necessary to mitigate these biases and prevent potential negative societal impacts.Future research should include a broader range of models for comparative analysis and explore more complex interactive scenarios to further understand and address these phenomena.The findings contribute significantly to understanding the limitations and capabilities of current AI systems,guiding their responsible development,and anticipating their potential societal implications.展开更多
Background Schizophrenia is characterised by pervasive cognitive deficits that significantly impair daily functioning and quality of life.Pharmacological treatments have limited efficacy in addressing these deficits,h...Background Schizophrenia is characterised by pervasive cognitive deficits that significantly impair daily functioning and quality of life.Pharmacological treatments have limited efficacy in addressing these deficits,highlighting the need for adjunctive interventions like computerised cognitive training(CCT).Aims This study aimed to evaluate the effects of a 30-session CCT programme on mental well-being and cognitive performance in individuals with schizophrenia.Additionally,it assessed the usability and acceptability of CCT in this population.Methods A double-blind,randomised clinical trial was conducted with 54 participants assigned to intervention and control groups.Cognitive and mental health outcomes were assessed using validated tools such as the Depression Anxiety Stress Scale 21,the Warwick-Edinburgh Mental Wellbeing Scale and the Cambridge Neuropsychological Test Automated Battery.Usability was measured with the System Usability Scale(SUS).Assessments were conducted at baseline,post-intervention and 3 months post-follow-up.Results The CCT intervention significantly improved mental well-being,reduced stress and enhanced working memory(paired associate learning,spatial working memory and spatial span)compared with controls.However,no significant effects were observed for anxiety,depression or executive function.Usability scores were high(SUS=83.51),and compliance rates were strong(92.7%),indicating favourable participant engagement.Conclusion CCT demonstrated potential as an adjunctive treatment for schizophrenia,with significant improvements in targeted cognitive and mental health domains.The high usability and compliance rates support its feasibility for broader implementation.Further research is needed to optimise protocols and explore long-term benefits.CCT offers a promising approach to addressing mental health and cognitive challenges in schizophrenia,particularly for stress and working memory.Its usability and acceptability suggest it could be seamlessly integrated into clinical practice.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
As drivers age, roadway conditions may become more challenging, particularly when normal aging is coupled with cognitive decline. Driving during lower visibility conditions, such as inclement weather, is especially ch...As drivers age, roadway conditions may become more challenging, particularly when normal aging is coupled with cognitive decline. Driving during lower visibility conditions, such as inclement weather, is especially challenging for older drivers due to their sensitivity to glare and reduced visibility. As a result, older drivers may adjust their behavior during adverse weather. This paper explores the differential impacts of weather on older drivers with cognitive decline compared to older drivers with normal cognitive function. Data were from a naturalistic driving study of older drivers in Omaha, Nebraska. Driver speed and weather data were extracted and the correlation between speed compliance, road weather conditions, and the cognitive/neurological status of the drivers was examined. Speed compliance was used as the surrogate safety measure since driving at lower speeds can indicate that the driver is challenged by roadway or environmental conditions and can therefore indicate a risk. The percentage of time during a trip when drivers were 16.1 kph under the speed limit was modeled as the dependent variable using beta regression. The variables that resulted in the best fit model were mild cognitive impairment (MCI), age group, traffic density, and weather. Results indicated that the youngest group of older drivers (young-old) spent less time driving at impeding speeds and had the least variability compared to the other two age groups. The middle group of older drivers (middle-old) had the highest amount of time driving at impeding speeds and had more variability than young-old drivers. The oldest group of older drivers (old-old) were the most likely to drive at impeding speeds and had the most variability. In general, older drivers were more likely to drive at impeding speeds during peak hours than during non-peak hours. Additionally, in most cases, older drivers spent less time below the speed limit when the weather was clear than in adverse conditions. Results indicate that older drivers are impacted by weather conditions, and distinct patterns were noted between older drivers who were cognitively impaired compared to drivers with normal cognition.展开更多
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 ...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.展开更多
文摘The concept of the brain cognitive reserve is derived from the well-acknowledged notion that the degree of brain damage does not always match the severity of clinical symptoms and neurological/cognitive outcomes.It has been suggested that the size of the brain(brain reserve) and the extent of neural connections acquired through life(neural reserve) set a threshold beyond which noticeable impairments occur.In contrast,cognitive reserve refers to the brain's ability to adapt and reo rganize stru cturally and functionally to resist damage and maintain function,including neural reserve and brain maintenance,resilience,and compensation(Verkhratsky and Zorec,2024).
基金supported by The Basic Science Research Program through the National Research Foundation of Korea(NRF)funded by the Ministry of Education(RS-2023-00244901)(to RB)。
文摘Challenges in the prevention and treatment of mild cognitive impairment associated with Alzheimer's disease:Increased life expectancy due to advancements in medical care has given rise to an aging population,accompanied by a surge in the incidence of incurable neurodegenerative diseases(NDDs).These diseases primarily affect the cognitive and behavioral functions of older adults by impacting brain activity.Mild cognitive impairment(MCI)is a neurodegenerative condition that affects a significant portion of the population.
基金supported by STI 2030-Major Projects,No.2021ZD0201603(to JL)the Joint Foundation Program of the Chinese Academy of Sciences,No.8091A170201(to JL)+1 种基金the National Natural Science Foundation of China,Nos.T2293730(to XC),T2293731(to XC),T2293734(to XC),62471291(to YW),62121003(to XC),61960206012(to XC),62333020(to XC),and 62171434(to XC)the National Key Research and Development Program of China,Nos.2022YFC2402501(to XC),2022YFB3205602(to XC).
文摘Neuromodulation techniques effectively intervene in cognitive function,holding considerable scientific and practical value in fields such as aerospace,medicine,life sciences,and brain research.These techniques utilize electrical stimulation to directly or indirectly target specific brain regions,modulating neural activity and influencing broader brain networks,thereby regulating cognitive function.Regulating cognitive function involves an understanding of aspects such as perception,learning and memory,attention,spatial cognition,and physical function.To enhance the application of cognitive regulation in the general population,this paper reviews recent publications from the Web of Science to assess the advancements and challenges of invasive and non-invasive stimulation methods in modulating cognitive functions.This review covers various neuromodulation techniques for cognitive intervention,including deep brain stimulation,vagus nerve stimulation,and invasive methods using microelectrode arrays.The non-invasive techniques discussed include transcranial magnetic stimulation,transcranial direct current stimulation,transcranial alternating current stimulation,transcutaneous electrical acupoint stimulation,and time interference stimulation for activating deep targets.Invasive stimulation methods,which are ideal for studying the pathogenesis of neurological diseases,tend to cause greater trauma and have been less researched in the context of cognitive function regulation.Non-invasive methods,particularly newer transcranial stimulation techniques,are gentler and more appropriate for regulating cognitive functions in the general population.These include transcutaneous acupoint electrical stimulation using acupoints and time interference methods for activating deep targets.This paper also discusses current technical challenges and potential future breakthroughs in neuromodulation technology.It is recommended that neuromodulation techniques be combined with neural detection methods to better assess their effects and improve the accuracy of non-invasive neuromodulation.Additionally,researching closed-loop feedback neuromodulation methods is identified as a promising direction for future development.
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.
文摘Complex genetic relationships between neurodegenerative disorders and neuropsychiatric symptoms have been shown, suggesting shared pathogenic mechanisms and emphasizing the potential for developing common therapeutic targets. Apolipoprotein E(APOE) genotypes and their corresponding protein(Apo E) isoforms may influence the biophysical properties of the cell membrane lipid bilayer. However, the role of APOE in central nervous system pathophysiology extended beyond its lipid transport function. In the present review article, we analyzed the links existing between APOE genotypes and the neurobiology of neuropsychiatric symptoms in neurodegenerative and vascular diseases. APOE genotypes(APOE ε2, APOE ε3, and APOE ε4) were implicated in common mechanisms underlying a wide spectrum of neurodegenerative diseases, including sporadic Alzheimer's disease, synucleinopathies such as Parkinson's disease and Lewy body disease, stroke, and traumatic brain injury. These shared pathways often involved neuroinflammation, abnormal protein accumulation, or responses to acute detrimental events. Across these conditions, APOE variants are believed to contribute to the modulation of inflammatory responses, the regulation of amyloid and tau pathology, as well as the clearance of proteins such as α-synuclein. The bidirectional interactions among Apo E, amyloid and mitochondrial metabolism, immunomodulatory effects, neuronal repair, and remodeling underscored the complexity of Apo E's role in neuropsychiatric symptoms associated with these conditions since from early phases of cognitive impairment such as mild cognitive impairment and mild behavioral impairment. Besides Apo E-specific isoforms' link to increased neuropsychiatric symptoms in Alzheimer's disease(depression, psychosis, aberrant motor behaviors, and anxiety, not apathy), the APOE ε4 genotype was also considered a significant genetic risk factor for Lewy body disease and its worse cognitive outcomes. Conversely, the APOE ε2 variant has been observed not to exert a protective effect equally in all neurodegenerative diseases. Specifically, in Lewy body disease, this variant may delay disease onset, paralleling its protective role in Alzheimer's disease, although its role in frontotemporal dementia is uncertain. The APOE ε4 genotype has been associated with adverse cognitive outcomes across other various neurodegenerative conditions. In Parkinson's disease, the APOE ε4 allele significantly impacted cognitive performance, increasing the risk of developing dementia, even in cases of pure synucleinopathies with minimal co-pathology from Alzheimer's disease. Similarly, in traumatic brain injury, recovery rates varied, with APOE ε4 carriers demonstrating a greater risk of poor long-term cognitive outcomes and elevated levels of neuropsychiatric symptoms. Furthermore, APOE ε4 influenced the age of onset and severity of stroke, as well as the likelihood of developing stroke-associated dementia, potentially due to its role in compromising endothelial integrity and promoting blood–brain barrier dysfunction.
基金supported by the Haihe Laboratory of Cell Ecosystem Innovation Foundation,No.22HHXBSS00047(to PL)Graduate Science and Technology Innovation Project of Tianjin,No.2022BKY173(to LZ)Tianjin Municipal Science and Technology Bureau Foundation,No.20201194(to PL).
文摘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.
文摘BACKGROUND Cognitive frailty and depression are prevalent among the elderly,significantly impairing physical and cognitive functions,psychological well-being,and quality of life.Effective interventions are essential to mitigate these adverse effects and enhance overall health outcomes in this population.AIM To evaluate the effects of exercise-cognitive dual-task training on frailty,cognitive function,psychological status,and quality of life in elderly patients with cognitive frailty and depression.METHODS A retrospective study was conducted on 130 patients with cognitive frailty and depression admitted between December 2021 and December 2023.Patients were divided into a control group receiving routine intervention and an observation group undergoing exercise-cognitive dual-task training in addition to routine care.Frailty,cognitive function,balance and gait,psychological status,and quality of life were assessed before and after the intervention.RESULTS After the intervention,the frailty score of the observation group was(5.32±0.69),lower than that of the control group(5.71±0.55).The Montreal cognitive assessment basic scale score in the observation group was(24.06±0.99),higher than the control group(23.43±1.40).The performance oriented mobility assessment score in the observation group was(21.81±1.24),higher than the control group(21.15±1.26).The self-efficacy in the observation group was(28.27±2.66),higher than the control group(30.05±2.66).The anxiety score in the hospital anxiety and depression scale(HADS)for the observation group was(5.86±0.68),lower than the control group(6.21±0.64).The depression score in the HADS for the observation group was(5.67±0.75),lower than the control group(6.27±0.92).Additionally,the scores for each dimension of the 36-item short form survey in the observation group were higher than those in the control group,with statistically significant differences(P<0.05).CONCLUSION Exercise-cognitive dual-task training is beneficial for improving frailty,enhancing cognitive function,and improving psychological status and quality of life in elderly patients with cognitive frailty and depression.
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 National Natural Science Foundation of China,No.82001155(to LL)the Natural Science Foundation of Zhejiang Province,No.LY23H090004(to LL)+5 种基金the Natural Science Foundation of Ningbo,No.2023J068(to LL)the Fundamental Research Funds for the Provincial Universities of Zhejiang Province,No.SJLY2023008(to LL)the College Students'Scientific and Technological Innovation Project(Xin Miao Talent Plan)of Zhejiang Province,No.2022R405A045(to CC)the Student ResearchInnovation Program(SRIP)of Ningbo University,Nos.20235RIP1919(to CZ),2023SRIP1938(to YZ)the K.C.Wong Magna Fund in Ningbo University。
文摘A reduction in adult neurogenesis is associated with behavioral abnormalities in patients with Alzheimer's disease.Consequently,enhancing adult neurogenesis represents a promising therapeutic approach for mitigating disease symptoms and progression.Nonetheless,nonpharmacological interventions aimed at inducing adult neurogenesis are currently limited.Although individual non-pharmacological interventions,such as aerobic exercise,acousto-optic stimulation,and olfactory stimulation,have shown limited capacity to improve neurogenesis and cognitive function in patients with Alzheimer's disease,the therapeutic effect of a strategy that combines these interventions has not been fully explored.In this study,we observed an age-dependent decrease in adult neurogenesis and a concurrent increase in amyloid-beta accumulation in the hippocampus of amyloid precursor protein/presenilin 1 mice aged 2-8 months.Amyloid deposition became evident at 4 months,while neurogenesis declined by 6 months,further deteriorating as the disease progressed.However,following a 4-week multifactor stimulation protocol,which encompassed treadmill running(46 min/d,10 m/min,6 days per week),40 Hz acousto-optic stimulation(1 hour/day,6 days/week),and olfactory stimulation(1 hour/day,6 days/week),we found a significant increase in the number of newborn cells(5'-bromo-2'-deoxyuridine-positive cells),immature neurons(doublecortin-positive cells),newborn immature neurons(5'-bromo-2'-deoxyuridine-positive/doublecortin-positive cells),and newborn astrocytes(5'-bromo-2'-deoxyuridine-positive/glial fibrillary acidic protein-positive cells).Additionally,the amyloid-beta load in the hippocampus decreased.These findings suggest that multifactor stimulation can enhance adult hippocampal neurogenesis and mitigate amyloid-beta neuropathology in amyloid precursor protein/presenilin 1 mice.Furthermore,cognitive abilities were improved,and depressive symptoms were alleviated in amyloid precursor protein/presenilin 1 mice following multifactor stimulation,as evidenced by Morris water maze,novel object recognition,forced swimming test,and tail suspension test results.Notably,the efficacy of multifactor stimulation in consolidating immature neurons persisted for at least 2weeks after treatment cessation.At the molecular level,multifactor stimulation upregulated the expression of neuron-related proteins(NeuN,doublecortin,postsynaptic density protein-95,and synaptophysin),anti-apoptosis-related proteins(Bcl-2 and PARP),and an autophagyassociated protein(LC3B),while decreasing the expression of apoptosis-related proteins(BAX and caspase-9),in the hippocampus of amyloid precursor protein/presenilin 1 mice.These observations might be attributable to both the brain-derived neurotrophic factor-mediated signaling pathway and antioxidant pathways.Furthermore,serum metabolomics analysis indicated that multifactor stimulation regulated differentially expressed metabolites associated with cell apoptosis,oxidative damage,and cognition.Collectively,these findings suggest that multifactor stimulation is a novel non-invasive approach for the prevention and treatment of Alzheimer's disease.
文摘Cognitive bias,stemming from electronic measurement error and variability in human perception,exists in cognitive electronic warfare and affects the outcomes of conflicts.In this paper,the dynamic game approach is employed to develop a model for cognitive bias induced by incomplete information and measurement errors in cognitive radar countermeasures.The payoffs for both parties are calculated using the radar's anti-jamming strategy matrix A and the jammer's jamming strategy matrix B.With perfect Bayesian equilibrium,a dynamic radar countermeasure model is established,and the impact of cognitive bias is analyzed.Drawing inspiration from the cognitive bias analysis method used in stock market trading,a cognitive bias model for cognitive radar countermeasures is introduced,and its correctness is mathematically proved.A gaming scenario involving the AN/SPY-1 radar and a smart jammer is set up to analyze the influence of cognitive bias on game outcomes.Simulation results validate the effectiveness of the proposed method.
基金supported by the Scientific Research Project of China Rehabilitation Research Center,No.2021zx-23the National Natural Science Foundation of China,No.32100925the Beijing Nova Program,No.Z211100002121038。
文摘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.
文摘BACKGROUND Mild cognitive impairment(MCI)has a high risk of progression to Alzheimer’s disease.The disease is often accompanied by sleep disorders,and whether sleep disorders have an effect on brain function in patients with MCI is unclear.AIM To explore the near-infrared brain function characteristics of MCI with sleep disorders.METHODS A total of 120 patients with MCI(MCI group)and 50 healthy subjects(control group)were selected.All subjects underwent the functional near-infrared spec-troscopy test.Collect baseline data,Mini-Mental State Examination,Montreal Cognitive Assessment scale,fatigue severity scale(FSS)score,sleep parameter,and oxyhemoglobin(Oxy-Hb)concentration and peak time of functional near-infrared spectroscopy test during the task period.The relationship between Oxy-RESULTS Compared with the control group,the FSS score of the MCI group was higher(t=11.310),and the scores of Pittsburgh sleep quality index,sleep time,sleep efficiency,nocturnal sleep disturbance,and daytime dysfunction were higher(Z=-10.518,-10.368,-9.035,-10.661,-10.088).Subjective sleep quality and total sleep time scores were lower(Z=-11.592,-9.924).The sleep efficiency of the MCI group was lower,and the awakening frequency,rem sleep latency period,total sleep time,and oxygen desaturation index were higher(t=5.969,5.829,2.887,3.003,5.937).The Oxy-Hb concentration at T0,T1,and T2 in the MCI group was lower(t=14.940,11.280,5.721),and the peak time was higher(t=18.800,13.350,9.827).In MCI patients,the concentration of Oxy-Hb during T0 was negatively correlated with the scores of Pittsburgh sleep quality index,sleep time,total sleep time,and sleep efficiency(r=-0.611,-0.388,-0.563,-0.356).It was positively correlated with sleep efficiency and total sleep time(r=0.754,0.650),and negatively correlated with oxygen desaturation index(r=-0.561)and FSS score(r=-0.526).All comparisons were P<0.05.CONCLUSION Patients with MCI and sleep disorders have lower near-infrared brain function than normal people,which is related to sleep quality.Clinically,a comprehensive assessment of the near-infrared brain function of patients should be carried out to guide targeted treatment and improve curative effect.
基金supported by the Research Foundation for Talented Scholars of Fujian Medical University,No.XRCZX2018014(to DZ)Startup Fund for Scientific Research,Fujian Medical University,No.2019QH1017(to CW)the Natural Science Foundation of Fujian Province,China,Nos.2021J01693(to DZ),2021J02032(to ZCY)。
文摘Previous studies have shown that the compound(E)-2-(3,4-dihydroxystyryl)-3-hydroxy-4H-pyran-4-one(D30),a pyromeconic acid derivative,possesses antioxidant and anti-inflammatory properties,inhibits amyloid-β aggregation,and alleviates scopolamine-induced cognitive impairment,similar to the phase Ⅲ clinical drug resveratrol.In this study,we established a mouse model of Alzheimer's disease via intracerebroventricular injection of fibrillar amyloid-β to investigate the effect of D30 on fibrillar amyloid-β-induced neuropathology.Our results showed that D30 alleviated fibrillar amyloid-β-induced cognitive impairment,promoted fibrillar amyloid-β clearance from the hippocampus and cortex,suppressed oxidative stress,and inhibited activation of microglia and astrocytes.D30 also reversed the fibrillar amyloid-β-induced loss of dendritic spines and synaptic protein expression.Notably,we demonstrated that exogenous fibrillar amyloid-βintroduced by intracerebroventricular injection greatly increased galectin-3 expression levels in the brain,and this increase was blocked by D30.Considering the role of D30 in clearing amyloid-β,inhibiting neuroinflammation,protecting synapses,and improving cognition,this study highlights the potential of galectin-3 as a promising treatment target for patients with Alzheimer's disease.
基金Supported by Basic Science Research Program Through the National Research Foundation of Korea(NRF)Funded By the Ministry of Education,No.NRF-RS-2023-00237287.
文摘This manuscript explores the recent study by Cui et al which assessed the interplay between inflammatory cytokines and brain-derived neurotrophic factor(BDNF)levels in first-episode schizophrenia patients.The study revealed that higher levels of interleukin-6 and tumor necrosis factor-αcorrelated with reduced BDNF levels and poorer cognitive performance.Schizophrenia is a severe psy-chiatric disorder impacting approximately 1%of the global population,charac-terized by positive symptoms(hallucinations and delusions),negative symptoms(diminished motivation and cognitive impairments)and disorganized thoughts and behaviors.Emerging research highlights the role of BDNF as a potential biomarker for early diagnosis and therapeutic targeting.The findings from Cui et al’s study suggest that targeting neuroinflammation and enhancing BDNF levels may improve cognitive outcomes.Effective treatment approaches involve a com-bination of pharmacological and non-pharmacological interventions tailored to individual patient needs.Hence,monitoring cognitive and neuroinflammatory markers is essential for improving patient outcomes and quality of life.Conse-quently,this manuscript highlights the need for an integrated approach to schizo-phrenia management,considering both clinical symptoms and underlying neuro-biological changes.
文摘The rapid advancement of Artificial Intelligence(AI)and Large Language Models(LLMs)has led to their increasing integration into various domains,from text generation and translation to question-answering.However,a critical question remains:do these sophisticated models,much like humans,exhibit susceptibility to cognitive biases?Understanding the presence and nature of such biases in AI is paramount for assessing their reliability,enhancing their performance,and predicting their societal impact.This research specifically investigates the susceptibility of Google’s Gemini 1.5 Pro and DeepSeek,two prominent LLMs,to framing effects and confirmation bias.The study meticulously designed a series of experimental trials,systematically manipulating information proportions and presentation orders to evaluate these biases.In the framing effect experiment,a genetic testing decision-making scenario was constructed.The proportion of positive and negative information(e.g.,20%,50%,or 80%positive)and their presentation order were varied.The models’inclination towards undergoing genetic testing was recorded.For the confirmation bias experiment,two reports-one positive and one negative-about“RoboTaxi”autonomous vehicles were provided.The proportion of erroneous information within these reports(10%,30%,and 50%)and their presentation order were systematically altered,and the models’support for each report was assessed.The findings demonstrate that both Gemini 1.5 Pro and DeepSeek are susceptible to framing effects.In the genetic testing scenario,their decision-making was primarily influenced by the proportion of positive and negative information presented.When the proportion of positive information was higher,both models showed a greater inclination to recommend or proceed with genetic testing.Conversely,a higher proportion of negative information led to greater caution or a tendency not to recommend the testing.Importantly,the order in which this information was presented did not significantly influence their decisions in the framing effect scenarios.Regarding confirmation bias,the two models exhibited distinct behaviors.Gemini 1.5 Pro did not show an overall preference for either positive or negative reports.However,its judgments were significantly influenced by the order of information presentation,demonstrating a“recency effect,”meaning it tended to support the report presented later.The proportion of erroneous information within the reports had no significant impact on Gemini 1.5 Pro’s decisions.In contrast,DeepSeek exhibited an overall confirmation bias,showing a clear preference for positive reports.Similar to Gemini 1.5 Pro,DeepSeek’s decisions were also significantly affected by the order of information presentation,while the proportion of misinformation had no significant effect.These results reveal human-like cognitive vulnerabilities in advanced LLMs,highlighting critical challenges to their reliability and objectivity in decision-making processes.Gemini 1.5 Pro’s sensitivity to presentation order and DeepSeek’s general preference for positive information,coupled with its sensitivity to order,underscore the need for careful evaluation of potential cognitive biases during the development and application of AI.The study suggests that effective measures are necessary to mitigate these biases and prevent potential negative societal impacts.Future research should include a broader range of models for comparative analysis and explore more complex interactive scenarios to further understand and address these phenomena.The findings contribute significantly to understanding the limitations and capabilities of current AI systems,guiding their responsible development,and anticipating their potential societal implications.
基金supported by a grant from University of Social Welfare and Rehabilitation Sciences for the research expenses.
文摘Background Schizophrenia is characterised by pervasive cognitive deficits that significantly impair daily functioning and quality of life.Pharmacological treatments have limited efficacy in addressing these deficits,highlighting the need for adjunctive interventions like computerised cognitive training(CCT).Aims This study aimed to evaluate the effects of a 30-session CCT programme on mental well-being and cognitive performance in individuals with schizophrenia.Additionally,it assessed the usability and acceptability of CCT in this population.Methods A double-blind,randomised clinical trial was conducted with 54 participants assigned to intervention and control groups.Cognitive and mental health outcomes were assessed using validated tools such as the Depression Anxiety Stress Scale 21,the Warwick-Edinburgh Mental Wellbeing Scale and the Cambridge Neuropsychological Test Automated Battery.Usability was measured with the System Usability Scale(SUS).Assessments were conducted at baseline,post-intervention and 3 months post-follow-up.Results The CCT intervention significantly improved mental well-being,reduced stress and enhanced working memory(paired associate learning,spatial working memory and spatial span)compared with controls.However,no significant effects were observed for anxiety,depression or executive function.Usability scores were high(SUS=83.51),and compliance rates were strong(92.7%),indicating favourable participant engagement.Conclusion CCT demonstrated potential as an adjunctive treatment for schizophrenia,with significant improvements in targeted cognitive and mental health domains.The high usability and compliance rates support its feasibility for broader implementation.Further research is needed to optimise protocols and explore long-term benefits.CCT offers a promising approach to addressing mental health and cognitive challenges in schizophrenia,particularly for stress and working memory.Its usability and acceptability suggest it could be seamlessly integrated into clinical practice.
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.
文摘As drivers age, roadway conditions may become more challenging, particularly when normal aging is coupled with cognitive decline. Driving during lower visibility conditions, such as inclement weather, is especially challenging for older drivers due to their sensitivity to glare and reduced visibility. As a result, older drivers may adjust their behavior during adverse weather. This paper explores the differential impacts of weather on older drivers with cognitive decline compared to older drivers with normal cognitive function. Data were from a naturalistic driving study of older drivers in Omaha, Nebraska. Driver speed and weather data were extracted and the correlation between speed compliance, road weather conditions, and the cognitive/neurological status of the drivers was examined. Speed compliance was used as the surrogate safety measure since driving at lower speeds can indicate that the driver is challenged by roadway or environmental conditions and can therefore indicate a risk. The percentage of time during a trip when drivers were 16.1 kph under the speed limit was modeled as the dependent variable using beta regression. The variables that resulted in the best fit model were mild cognitive impairment (MCI), age group, traffic density, and weather. Results indicated that the youngest group of older drivers (young-old) spent less time driving at impeding speeds and had the least variability compared to the other two age groups. The middle group of older drivers (middle-old) had the highest amount of time driving at impeding speeds and had more variability than young-old drivers. The oldest group of older drivers (old-old) were the most likely to drive at impeding speeds and had the most variability. In general, older drivers were more likely to drive at impeding speeds during peak hours than during non-peak hours. Additionally, in most cases, older drivers spent less time below the speed limit when the weather was clear than in adverse conditions. Results indicate that older drivers are impacted by weather conditions, and distinct patterns were noted between older drivers who were cognitively impaired compared to drivers with normal cognition.
基金supported by the National Natural Science Foundation of China,Nos.81730033,82171193(to XG)the Key Talent Project for Strengthening Health during the 13^(th)Five-Year Plan Period,No.ZDRCA2016069(to XG)+1 种基金the National Key R&D Program of China,No.2018YFC2001901(to XG)Jiangsu Provincial Medical Key Discipline,No.ZDXK202232(to XG)。
文摘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.
