Current Alzheimer research最新文献

{"title":"Environmental Enrichment and Metformin Combination Improves Cognitive Function through BDNF and HPA Axis in Chronically Stressed Rats.","authors":"V Bhagya, K Tilak, L Kanimozhi, R Sushma","doi":"10.2174/0115672050379003250520072717","DOIUrl":"https://doi.org/10.2174/0115672050379003250520072717","url":null,"abstract":"<p><strong>Introduction: </strong>Chronic stress is a major global health issue linked to conditions such as anxiety, depression, and cognitive decline. In rodent studies, chronic immobilization stress (CIS) is commonly used to investigate the neuropsychological effects of prolonged stress, leading to behaviours such as anhedonia, anxiety, and depressive-like symptoms. An enriched environment (EE) provides physical, cognitive, and sensory stimulation, which promotes social interaction, supports brain development, and can enhance the effectiveness of pharmacological treatments, improving overall therapeutic outcomes. Metformin, commonly prescribed for type 2 diabetes, has antidiabetic effects and helps reduce oxidative stress, inflammation, and cell death in the brain, which may contribute to its neuroprotective properties. This study aims to evaluate the effectiveness of metformin, an enriched environment (EE), and its combination in alleviating anxiety and depression-like behaviours, memory impairments, and metabolic changes.</p><p><strong>Materials and methods: </strong>Rats were exposed to chronic immobilization stress (CIS) for 2 hours per day over a period of 10 days, followed by 14 days of treatment with metformin (200 mg/kg) and 6 hours of daily exposure to an enriched environment (EE). Behavioural tests, including the open field test (OFT), elevated plus maze (EPM), sucrose preference test (SPT), and novel object recognition test (NORT), were conducted. After completing the behavioural assessments, the animals were euthanized, and their plasma levels of corticosterone (CORT), high-density lipoprotein (HDL), low-density lipoprotein (LDL), cholesterol, triglycerides, and glucose were measured. Additionally, the concentration of brainderived neurotrophic factor (BDNF) in the hippocampus was analysed.</p><p><strong>Results: </strong>Rats exposed to chronic immobilization stress (CIS) exhibited increased anxiety and depressive- like behaviours, as well as poor performance in the novel object recognition test (NORT). These behavioural changes were linked to elevated levels of plasma corticosterone (CORT), LDL, cholesterol, triglycerides, and glucose, along with decreased HDL levels and lower hippocampal BDNF. Treatment with metformin, an enriched environment (EE), or their combination alleviated these effects, improving exploratory behaviour, sucrose preference, and recognition memory and reducing anxiety-like behaviours. These benefits were accompanied by increased hippocampal BDNF expression, elevated plasma HDL, and reduced levels of CORT, LDL, cholesterol, triglycerides, and glucose.</p><p><strong>Discussion: </strong>The combination of metformin and an enriched environment completely restored cognitive impairment and metabolic alterations in chronic stress conditions. Metformin's ability to improve energy metabolism and reduce oxidative stress could be further enhanced in an enriched environment, which promotes cognitive function and resil","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144145373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predictive Value of Complete Blood Count Parameters for Alzheimer's Disease in Relation to Periodontal Status.","authors":"Kubra Karaduran, Ahmet Aydogdu, Ozlem Gelisin, Sadiye Gunpinar","doi":"10.2174/0115672050388220250511174043","DOIUrl":"https://doi.org/10.2174/0115672050388220250511174043","url":null,"abstract":"<p><strong>Introduction/objective: </strong>Given the role of inflammation in the development of both Alzheimer's disease (AD) and periodontal disease, it is plausible that periodontal disease may influence the progression of AD. Complete blood count (CBC) parameters may also serve as predictive indicators for this condition. This study investigated the predictive value of CBC parameters on the progression of AD in patients with periodontal disease.</p><p><strong>Methods: </strong>Data from a prospective cohort study (n=90) with 6-month follow-up was analyzed. AD was assessed based on the Clinical Dementia Rating Scale. Records of C-reactive Protein (CRP) levels and CBC parameters measured within the 6 months preceding the participation date were evaluated. Cognitive assessments at the initial and 6th-month follow-up were performed using the Standardized Mini-Mental Test (SMMT). All patients underwent clinical periodontal examination.</p><p><strong>Results: </strong>The difference in SMMT score change (ΔSMMT) and platelet distribution width (PDW) value between groups with and without periodontitis was statistically notable (p<0.05). The presence of periodontitis was found to be significantly associated with age, ΔSMMT, and PDW values using the multivariate logistic regression model (p<0.05). Furthermore, having Stage II and Stage III AD, periodontitis, age factor, and mean platelet volume (MPV) value had a notable impact on ΔSMMT (p<0.05).</p><p><strong>Conclusion: </strong>PDW and MPV levels may have a predictive significance in clarifying the association between periodontitis and AD progression.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association Between Serum Lipid Traits and Cognitive Function in Middle-aged and Elderly Adults: A Longitudinal Study.","authors":"Chuning Luo, Qin Li, Ran Gao, Yijun Zhang, Yijie Wang, Fengyi Huang, Quanmei Li, Xite Zheng, Xiaorui Zhang, Wanqi Liu, Fen Liu","doi":"10.2174/0115672050370810250430112549","DOIUrl":"10.2174/0115672050370810250430112549","url":null,"abstract":"<p><strong>Background: </strong>It is debatable whether demographic factors alter the relationship between serum lipid traits and cognitive function. Few data have examined the effects of non-traditional lipid metrics on the lipid-cognition relationship. We aim to test the generality of relationships between lipid traits and cognitive function in Chinese adults.</p><p><strong>Methods: </strong>Data from 5,959 participants were obtained from the China Health and Retirement Longitudinal Study (2011-2020). The cognitive function was assessed via the Mini-Mental State Examination. Effects of traditional lipid metrics (Total Cholesterol, TC, Triglycerides, TG, Low-Density Lipoprotein, LDL, High-Density Lipoprotein, HDL) and non-traditional lipid metrics (TC/HDL, LDL/HDL) were analyzed. We employed mixed-effect models, Group-Based Trajectory Models (GBTM), and logistic regression to examine the associations between baseline serum lipid traits and cognitive function.</p><p><strong>Results: </strong>As continuous variables, higher TG levels were correlated with higher cognitive scores (P=0.036), and similar patterns were found in TC/HDL (P < 0.01) and LDL/HDL (P < 0.01). In contrast, higher HDL levels were associated with lower cognitive scores. Similar trends were observed when lipid traits were analyzed as categorical quartiles, and grouped by gender and age. Non-traditional lipid metrics (LDL/HDL, TC/HDL) had higher contributions to the variation of cognitive scores than traditional lipid metrics (TC, TG, LDL, HDL).</p><p><strong>Conclusion: </strong>Our study provided evidence for the generality of a significant association between traditional/non-traditional lipid metrics and cognitive function in middle-aged and elderly adults. The factors that vary with genders and age groups do not appear to significantly alter the lipid-cognition relationship.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144083127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating the Relationships Between Neurodegenerative Diseases and Cancer Types: A Computational Approach.","authors":"Claudia Cava, Isabella Castiglioni","doi":"10.2174/0115672050389561250429112631","DOIUrl":"https://doi.org/10.2174/0115672050389561250429112631","url":null,"abstract":"<p><strong>Introduction: </strong>Previous studies have shown a correlation between neurodegenerative diseases and cancers. However, the biological processes for these diseases are not completely known, and the genetic factors for their onset are not defined.</p><p><strong>Materials and methods: </strong>This study reports the genetic relationships of different neurodegenerative diseases, such as Multiple Sclerosis (MS), Alzheimer's Disease (AD), and Parkinson's disease (PD) and cancer types (squamous cell lung carcinoma, esophageal adenocarcinoma, and colorectal cancer), with other human traits, based on cross-trait Linkage Disequilibrium Score regression (LDSC). We then applied a clumping approach to select candidate genes for each disease, and via an miRNA analysis, we identified miRNAs that could regulate those genes.</p><p><strong>Results: </strong>LDSC revealed an inverse association of human traits with neurodegenerative diseases and cancer. Indeed, the cancer types studied were positively correlated with \"Body Mass Index (BMI),\" while AD, PD, and MS showed a negative correlation. miR-1-3p, miR-34a-5p, and miR-27a-3p were revealed as common biomarkers among the different pathological conditions.</p><p><strong>Conclusion: </strong>The present study suggests novel genetic associations between neurological diseases, cancer types and new targets to explain the genetic sharing between the diseases.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144051536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Framework for an Integrative Theory of Alzheimer's Disease.","authors":"Dmitry V Zaretsky, Maria V Zaretskaia","doi":"10.2174/0115672050381553250425062803","DOIUrl":"https://doi.org/10.2174/0115672050381553250425062803","url":null,"abstract":"<p><p>The manuscript describes how the framework of the integrative hypothesis of Alzheimer's disease (AD) can be deciphered using existing experimental and clinical data. First, the analysis of amyloid biomarkers and stable-isotope label kinetics (SILK) studies indicate a correlation between AD diagnosis and heightened cellular uptake of beta-amyloid. Since beta-amyloid must be taken up by cells to become toxic, its uptake rate correlates with neurodegeneration. Also, aggregation seeds cannot form extracellularly due to low beta-amyloid levels in interstitial fluid but can develop inside lysosomes. Consequently, the density of extracellular aggregates correlates positively with cellular amyloid uptake rate. The model, which ties both beta-amyloid cytotoxicity and aggregation to cellular uptake, accurately predicts AD diagnosis patterns in the population. Second, beta-amyloid enters cells through endocytosis. Endocytosed beta-amyloid induces lysosomal permeabilization that occurs without plasma membrane damage and explains intracellular ion disturbances (including calcium overload) after exposure to extracellular beta-amyloid. The permeabilization is caused by channels formed in lysosomal membranes by some amyloid fragments produced by proteolysis of full-length beta-amyloid. Some membrane channels are large enough to leak cathepsins to the cytoplasm, causing necrosis or apoptosis. Also, local spikes of calcium cytosolic concentration due to calcium leakage from lysosomes can activate calpains, contributing to cell death. In surviving cells, accumulation of damaged lysosomes results in autophagy failure and slow mitochondrial recycling, promoting the production of reactive oxygen species and further cell damage. In this framework, AD's etiology is the membrane channel formation by amyloid fragments produced in lysosomes. The pathogenesis includes lysosomal permeabilization and the appearance of activated proteases in the cytoplasm. The correlation between AD diagnosis and the density of amyloid aggregates occurs because both amyloid cytotoxicity and extracellular aggregate formation stem from cellular amyloid uptake. To reflect key processes, we call this framework the Amyloid Degradation Toxicity Hypothesis of Alzheimer's Disease. It explains various phenomena and paradoxes associated with AD pathobiology across molecular, cellular, and biomarker levels. The hypothesis also highlights the limitations of current AD biomarkers and suggests new diagnostic and prognostic tools based on disease pathogenesis. Additionally, the framework identifies potential pharmacological targets for preventing disease progression.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144060801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the Role of Nutrition in Supporting Brain Health and Reducing the Risk of Alzheimer's Disease.","authors":"Saurabh RamBihariLal Shrivastava, Prateek Sudhakar Bobhate","doi":"10.2174/0115672050397848250425060101","DOIUrl":"https://doi.org/10.2174/0115672050397848250425060101","url":null,"abstract":"<p><p>Alzheimer's disease (AD) has been ranked as the most common cause of dementia worldwide, which makes it a major cause of public health concern. The development of AD has been linked to a combination of factors, among which lifestyle-related factors can be targeted to minimize the risk of AD. A balanced diet acts as a source of all essential nutrients that can facilitate the functioning of the brain, promote cognitive longevity, safeguard against neurodegeneration, and, accordingly, reduce the risk of AD. Despite the availability of conclusive evidence highlighting the role of nutrition in the prevention of AD, a range of concerns have been identified that limit dietary adherence and public health efforts. This calls for the need to adopt a multipronged approach, including interventions targeting policy-level changes, the education sector, improvement in the food systems, and behavioural modifications to encourage long-term adherence to diets that are healthy for the brain. In conclusion, diet plays a crucial role in Alzheimer's disease, and there arises the need to incorporate food items that are healthy for the brain to maintain cognitive health and reduce the overall risk. The available data suggests that food items rich in antioxidants, omega-3 fatty acids, and B vitamins are associated with a lower risk of developing Alzheimer's disease.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144049078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PREFACE.","authors":"Thomas V Groen","doi":"10.2174/0115672050409702250506055217","DOIUrl":"https://doi.org/10.2174/0115672050409702250506055217","url":null,"abstract":"","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144045728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Footprint of CHASERR as a Potential Culprit in Alzheimer's Disease Patients: An In-Silico-Experimental Study.","authors":"Zahra Khosroabadi, Anoosha Niazmand, Seyed Reza Mousavi, Neda Hosseini, Nastaran Bagheri, Ahmad Chitsaz, Mansoor Salehi","doi":"10.2174/0115672050381537250422075255","DOIUrl":"https://doi.org/10.2174/0115672050381537250422075255","url":null,"abstract":"<p><strong>Objectives: </strong>Dementia has become a major global cause of death, posing significant health and economic challenges. Alzheimer's disease (AD) is the most common type of dementia. Recent studies have shown that long noncoding RNAs (lncRNAs) play a role in AD development. In this context, the current study conducted a comprehensive meta-analysis of high-throughput Gene Expression Omnibus (GEO) datasets to identify significant lncRNAs that could play a crucial role in the pathogenesis of AD.</p><p><strong>Methods: </strong>Three microarray expression profiles of human subjects diagnosed with AD and corresponding healthy controls were obtained from the GEO database. Afterward, the expression profiles from the chosen microarray datasets were combined. A network of differentially expressed genes (DEGs) was visualized, identifying key hub genes. Subsequently, the two significant lncRNAs, identified as LINC01003 and CHASERR, were chosen based on the number of interactions between hubs and lncRNAs. Blood samples were collected from AD patients as well as from healthy control individuals. Ultimately, the expression levels of CHASERR and LINC01003 were quantitatively assessed in the blood samples of 50 AD patients and 50 healthy controls using the quantitative Real-Time PCR (q-PCR) technique.</p><p><strong>Results: </strong>Experimental validation showed that CHASERR was differentially expressed in Alzheimer's disease (AD) patients compared to the control group. In contrast, LINC01003 revealed no significant difference between the AD patients and the control group.</p><p><strong>Conclusion: </strong>This study thoroughly examined the molecular landscape of AD, identifying key differentially expressed genes and highlighting candidate CHASERR as a potential molecular biomarker for AD patients.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143996512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Social Isolation as a Risk Factor for Dementia: Insights from Animal Model Studies.","authors":"Wataru Araki","doi":"10.2174/0115672050373522250421054927","DOIUrl":"https://doi.org/10.2174/0115672050373522250421054927","url":null,"abstract":"<p><p>Social isolation (SI) and loneliness (perceived social isolation) are considered as risk factors for developing dementia, including Alzheimer's disease (AD), in the elderly population. Intriguingly, recent reports have shown a significant association of loneliness with a higher amyloid- β (Aβ) burden, suggesting that SI is linked to the pathophysiology of AD. Numerous studies, using rodents or other animal models have revealed diverse biological effects of SI, including induction of oxidative stress and activation of neuroinflammation. Furthermore, using transgenic mouse models of AD, recent investigations have shown that SI affects AD pathology, particularly the deposition of Aβ and neuroinflammation. However, it remains unclarified, by which mechanisms SI confers a significant risk for AD. In this narrative mini-review, I overview published studies on the pathobiological effects of SI in rodent models and discuss the mechanisms by which SI exacerbates AD pathology. Clarification of this issue has significant implications for the design of strategies for preventing cognitive impairment and dementia in the elderly population.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144030530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NRN1 may Modulate Tau Phosphorylation and Neuronal Apoptosis in AD via the PIGU-CASP3 Axis.","authors":"Wenshuo Cheng, Jia Zhang, Hui Zhu, Zhenyu Wang, Min Li, Junyi Wang, Hongdan Fu, Yutai Zhang, Changyu Chen, Yuhang Gao, Cunhu Yuan, Jingling Zhu, Jiawei Sun","doi":"10.2174/0115672050361366250328040542","DOIUrl":"https://doi.org/10.2174/0115672050361366250328040542","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by hyperphosphorylation of tau protein to form neurofibrillary tangles (NFTs) and amyloid β (Aβ) deposition to form senile plaques, and its specific regulatory mechanism remains incompletely understood. Neurotrophic factors (NTFs) play important roles in neuronal growth, differentiation, and survival, and are considered to have potential therapeutic effects in AD.</p><p><strong>Objective: </strong>This study aimed to investigate the effects of NTFs on tau protein phosphorylation in AD and its underlying mechanisms.</p><p><strong>Methods: </strong>A correlation analysis was conducted between neurotrophic factors and tau protein phosphorylation genes using bioinformatics analysis. The relationship between the candidate neurotrophic factor NRN1 and tau protein phosphorylation was validated in vivo. The effects of NRN1 on tau protein phosphorylation, neural process-related proteins, and apoptosis were explored in vitro. Subsequently, GO and KEGG pathway enrichment analyses and PPI network were utilized to identify potential functions and pathways, as well as pinpoint core regulatory factors. Finally, the mechanism by which NRN1 affects tau protein phosphorylation was explored through Western blot analysis.</p><p><strong>Results: </strong>Bioinformatics analysis revealed a significant negative correlation between NRN1 and MAPT, a gene linked to tau protein phosphorylation. Western blot analysis indicated a decrease in NRN1 expression and an increase in p-tau levels in the hippocampus of AD mice. NRN1 significantly reduced the expression of p-tau in AD cell models and enhanced the expression of MAP2, a protein related to neural processes. Further, apoptosis analysis demonstrated that NRN1 significantly decreased the level of cleaved caspase-3 and elevated the Bcl-2/Bax ratio. Bioinformatics analysis and PPI network construction suggested PIGU and CASP3 to play pivotal roles in NRN1 regulation of tau protein phosphorylation.</p><p><strong>Conclusion: </strong>NRN1 may mitigate tau protein phosphorylation and neuronal apoptosis by modulating the PIGU-CASP3 pathway in AD. This finding offers novel insights into NRN1 as a potential target for the treatment of AD.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144060259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}