Pub Date : 2024-09-13DOI: 10.3389/fnagi.2024.1397696
Yanxiu Ju, Songtao Li, Xiangyi Kong, Qing Zhao
IntroductionThe prediction of progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD) is an important clinical challenge. This study aimed to identify the independent risk factors and develop a nomogram model that can predict progression from MCI to AD.MethodsData of 141 patients with MCI were obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database. We set a follow-up time of 72 months and defined patients as stable MCI (sMCI) or progressive MCI (pMCI) according to whether or not the progression of MCI to AD occurred. We identified and screened independent risk factors by utilizing weighted gene co-expression network analysis (WGCNA), where we obtained 14,893 genes after data preprocessing and selected the soft threshold β = 7 at an <jats:italic>R</jats:italic><jats:sup>2</jats:sup> of 0.85 to achieve a scale-free network. A total of 14 modules were discovered, with the midnightblue module having a strong association with the prognosis of MCI. Using machine learning strategies, which included the least absolute selection and shrinkage operator and support vector machine-recursive feature elimination; and the Cox proportional-hazards model, which included univariate and multivariable analyses, we identified and screened independent risk factors. Subsequently, we developed a nomogram model for predicting the progression from MCI to AD. The performance of our nomogram was evaluated by the C-index, calibration curve, and decision curve analysis (DCA). Bioinformatics analysis and immune infiltration analysis were conducted to clarify the function of early B cell factor 1 (EBF1).ResultsFirst, the results showed that 40 differentially expressed genes (DEGs) related to the prognosis of MCI were generated by weighted gene co-expression network analysis. Second, five hub variables were obtained through the abovementioned machine learning strategies. Third, a low Montreal Cognitive Assessment (MoCA) score [hazard ratio (HR): 4.258, 95% confidence interval (CI): 1.994–9.091] and low EBF1 expression (hazard ratio: 3.454, 95% confidence interval: 1.813–6.579) were identified as the independent risk factors through the Cox proportional-hazards regression analysis. Finally, we developed a nomogram model including the MoCA score, EBF1, and potential confounders (age and gender). By evaluating our nomogram model and validating it in both internal and external validation sets, we demonstrated that our nomogram model exhibits excellent predictive performance. Through the Gene Ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes Genomes (KEGG) functional enrichment analysis, and immune infiltration analysis, we found that the role of EBF1 in MCI was closely related to B cells.ConclusionEBF1, as a B cell-specific transcription factor, may be a key target for predicting progression from MCI to AD. Our nomogram model was able to provide personalized risk factors for the progression from MCI to AD after evaluation and
导言：预测从轻度认知障碍（MCI）发展为阿尔茨海默病（AD）是一项重要的临床挑战。本研究旨在确定独立的风险因素，并建立一个能预测 MCI 向 AD 发展的提名图模型。方法从阿尔茨海默病神经影像学倡议（ADNI）数据库中获得了 141 名 MCI 患者的数据。我们将随访时间设定为 72 个月，并根据 MCI 是否进展为 AD 将患者定义为稳定型 MCI（sMCI）或进展型 MCI（pMCI）。我们通过加权基因共表达网络分析（WGCNA）来识别和筛选独立的风险因素，经过数据预处理后，我们得到了14893个基因，并选择了R2为0.85的软阈值β=7来实现无标度网络。共发现了 14 个模块，其中午夜蓝模块与 MCI 的预后密切相关。我们利用机器学习策略，包括最小绝对选择和收缩算子以及支持向量机递归特征消除；以及 Cox 比例危险模型，包括单变量和多变量分析，确定并筛选出了独立的危险因素。随后，我们建立了一个用于预测 MCI 向 AD 演进的提名图模型。我们通过C指数、校准曲线和决策曲线分析（DCA）对提名图的性能进行了评估。结果首先，通过加权基因共表达网络分析得出了40个与MCI预后相关的差异表达基因（DEGs）。其次，通过上述机器学习策略获得了五个中枢变量。第三，通过 Cox 比例危险度回归分析，确定蒙特利尔认知评估（MoCA）低评分[危险度比（HR）：4.258，95% 置信区间（CI）：1.994-9.091]和 EBF1 低表达（危险度比：3.454，95% 置信区间：1.813-6.579）为独立危险因素。最后，我们建立了一个包括 MoCA 评分、EBF1 和潜在混杂因素（年龄和性别）的提名图模型。通过对我们的提名图模型进行评估，并在内部和外部验证集中进行验证，我们证明了我们的提名图模型具有出色的预测性能。通过基因本体（GO）富集分析、京都基因组百科全书（KEGG）功能富集分析和免疫浸润分析，我们发现 EBF1 在 MCI 中的作用与 B 细胞密切相关。经过评估和验证，我们的提名图模型能够提供从 MCI 发展为 AD 的个性化风险因素。
{"title":"EBF1 is a potential biomarker for predicting progression from mild cognitive impairment to Alzheimer's disease: an in silico study","authors":"Yanxiu Ju, Songtao Li, Xiangyi Kong, Qing Zhao","doi":"10.3389/fnagi.2024.1397696","DOIUrl":"https://doi.org/10.3389/fnagi.2024.1397696","url":null,"abstract":"IntroductionThe prediction of progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD) is an important clinical challenge. This study aimed to identify the independent risk factors and develop a nomogram model that can predict progression from MCI to AD.MethodsData of 141 patients with MCI were obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database. We set a follow-up time of 72 months and defined patients as stable MCI (sMCI) or progressive MCI (pMCI) according to whether or not the progression of MCI to AD occurred. We identified and screened independent risk factors by utilizing weighted gene co-expression network analysis (WGCNA), where we obtained 14,893 genes after data preprocessing and selected the soft threshold β = 7 at an <jats:italic>R</jats:italic><jats:sup>2</jats:sup> of 0.85 to achieve a scale-free network. A total of 14 modules were discovered, with the midnightblue module having a strong association with the prognosis of MCI. Using machine learning strategies, which included the least absolute selection and shrinkage operator and support vector machine-recursive feature elimination; and the Cox proportional-hazards model, which included univariate and multivariable analyses, we identified and screened independent risk factors. Subsequently, we developed a nomogram model for predicting the progression from MCI to AD. The performance of our nomogram was evaluated by the C-index, calibration curve, and decision curve analysis (DCA). Bioinformatics analysis and immune infiltration analysis were conducted to clarify the function of early B cell factor 1 (EBF1).ResultsFirst, the results showed that 40 differentially expressed genes (DEGs) related to the prognosis of MCI were generated by weighted gene co-expression network analysis. Second, five hub variables were obtained through the abovementioned machine learning strategies. Third, a low Montreal Cognitive Assessment (MoCA) score [hazard ratio (HR): 4.258, 95% confidence interval (CI): 1.994–9.091] and low EBF1 expression (hazard ratio: 3.454, 95% confidence interval: 1.813–6.579) were identified as the independent risk factors through the Cox proportional-hazards regression analysis. Finally, we developed a nomogram model including the MoCA score, EBF1, and potential confounders (age and gender). By evaluating our nomogram model and validating it in both internal and external validation sets, we demonstrated that our nomogram model exhibits excellent predictive performance. Through the Gene Ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes Genomes (KEGG) functional enrichment analysis, and immune infiltration analysis, we found that the role of EBF1 in MCI was closely related to B cells.ConclusionEBF1, as a B cell-specific transcription factor, may be a key target for predicting progression from MCI to AD. Our nomogram model was able to provide personalized risk factors for the progression from MCI to AD after evaluation and ","PeriodicalId":12450,"journal":{"name":"Frontiers in Aging Neuroscience","volume":"3 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142267361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-13DOI: 10.3389/fnagi.2024.1415072
Amy Christensen, Cassandra J. McGill, Wenjie Qian, Christian J. Pike
The main genetic risk factor for Alzheimer’s disease (AD) is the apolipoprotein E ε4 allele (APOE4). AD risk associated with APOE4 disproportionately affects women. Furthermore, human and rodent studies indicate that the cognitive deficits associated with APOE4 are greater in females. One modifiable AD risk factor is obesity during middle age. Given that approximately two-thirds of US adults are overweight, it is important to understand how obesity affects AD risk, how it interacts with APOE4, and the extent to which its detrimental effects can be mitigated with therapeutics. One intervention study for women is estrogen-based hormone therapy, which can exert numerous health benefits when administered in early middle age. No experimental studies have examined the interactions among APOE4, obesity, and hormone therapy in aging females. To begin to explore these issues, we considered how obesity outcomes are affected by treatment with estradiol at the onset of middle age in female mice with human APOE3 and APOE4. Furthermore, to explore how gene dosage affects outcomes, we compared mice homozygous for APOE3 (3/3) and homozygous (4/4) or hemizygous (3/4) for APOE4. Mice were examined over a 4-month period that spans the transition into reproductive senescence, a normal age-related change that models many aspects of human perimenopause. Beginning at 5 months of age, mice were maintained on a control diet (10% fat) or high-fat diet (HFD; 60% fat). After 8 weeks, by which time obesity was present in all HFD groups, mice were implanted with an estradiol or vehicle capsule that was maintained for the final 8 weeks. Animals were assessed on a range of metabolic and neural measures. Overall, APOE4 was associated with poorer metabolic function and cognitive performance. However, an obesogenic diet induced relatively greater impairments in metabolic function and cognitive performance in APOE3/3 mice. Estradiol treatment improved metabolic and cognitive outcomes across all HFD groups, with APOE4/4 generally exhibiting the greatest benefit. APOE3/4 mice were intermediate to the homozygous genotypes on many measures but also exhibited unique profiles. Together, these findings highlight the importance of the APOE genotype as a modulator of the risks associated with obesity and the beneficial outcomes of estradiol.
{"title":"Effects of obesogenic diet and 17β-estradiol in female mice with APOE 3/3, 3/4, and 4/4 genotypes","authors":"Amy Christensen, Cassandra J. McGill, Wenjie Qian, Christian J. Pike","doi":"10.3389/fnagi.2024.1415072","DOIUrl":"https://doi.org/10.3389/fnagi.2024.1415072","url":null,"abstract":"The main genetic risk factor for Alzheimer’s disease (AD) is the apolipoprotein E ε4 allele (<jats:italic>APOE4</jats:italic>). AD risk associated with <jats:italic>APOE4</jats:italic> disproportionately affects women. Furthermore, human and rodent studies indicate that the cognitive deficits associated with <jats:italic>APOE4</jats:italic> are greater in females. One modifiable AD risk factor is obesity during middle age. Given that approximately two-thirds of US adults are overweight, it is important to understand how obesity affects AD risk, how it interacts with <jats:italic>APOE4</jats:italic>, and the extent to which its detrimental effects can be mitigated with therapeutics. One intervention study for women is estrogen-based hormone therapy, which can exert numerous health benefits when administered in early middle age. No experimental studies have examined the interactions among <jats:italic>APOE4</jats:italic>, obesity, and hormone therapy in aging females. To begin to explore these issues, we considered how obesity outcomes are affected by treatment with estradiol at the onset of middle age in female mice with human <jats:italic>APOE3</jats:italic> and <jats:italic>APOE4</jats:italic>. Furthermore, to explore how gene dosage affects outcomes, we compared mice homozygous for <jats:italic>APOE3</jats:italic> (3/3) and homozygous (4/4) or hemizygous (3/4) for <jats:italic>APOE4</jats:italic>. Mice were examined over a 4-month period that spans the transition into reproductive senescence, a normal age-related change that models many aspects of human perimenopause. Beginning at 5 months of age, mice were maintained on a control diet (10% fat) or high-fat diet (HFD; 60% fat). After 8 weeks, by which time obesity was present in all HFD groups, mice were implanted with an estradiol or vehicle capsule that was maintained for the final 8 weeks. Animals were assessed on a range of metabolic and neural measures. Overall, <jats:italic>APOE4</jats:italic> was associated with poorer metabolic function and cognitive performance. However, an obesogenic diet induced relatively greater impairments in metabolic function and cognitive performance in <jats:italic>APOE3/3</jats:italic> mice. Estradiol treatment improved metabolic and cognitive outcomes across all HFD groups, with <jats:italic>APOE4/4</jats:italic> generally exhibiting the greatest benefit. <jats:italic>APOE3/4</jats:italic> mice were intermediate to the homozygous genotypes on many measures but also exhibited unique profiles. Together, these findings highlight the importance of the <jats:italic>APOE</jats:italic> genotype as a modulator of the risks associated with obesity and the beneficial outcomes of estradiol.","PeriodicalId":12450,"journal":{"name":"Frontiers in Aging Neuroscience","volume":"9 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142267194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-12DOI: 10.3389/fnagi.2024.1438367
Shuo Liu, Tao Bai, Juan Feng
Endothelial cell specific-1 (ESM-1), also known as endocan, is a soluble dermatan sulfate proteoglycan that is mainly secreted by endothelial cells. Endocan is associated with tumorigenesis and cancer progression and is also related to cardiovascular disorders, autoimmune diseases, and sepsis. The phenylalanine-rich region and linear polysaccharide of endocan are necessary for the protein to exert its biological functions. Elevated plasma endocan levels reflect endothelial activation and dysfunction. In addition, endocan participates in complex inflammatory responses and proliferative processes. Here, we reviewed current research on endocan, elaborated the protein’s structure and biological functions, and speculated on its possible clinical value in nervous system diseases. We conclude that endocan may be a glycoprotein that plays an important role in neurological disorders.
{"title":"Endocan, a novel glycoprotein with multiple biological activities, may play important roles in neurological diseases","authors":"Shuo Liu, Tao Bai, Juan Feng","doi":"10.3389/fnagi.2024.1438367","DOIUrl":"https://doi.org/10.3389/fnagi.2024.1438367","url":null,"abstract":"Endothelial cell specific-1 (<jats:italic>ESM-1</jats:italic>), also known as endocan, is a soluble dermatan sulfate proteoglycan that is mainly secreted by endothelial cells. Endocan is associated with tumorigenesis and cancer progression and is also related to cardiovascular disorders, autoimmune diseases, and sepsis. The phenylalanine-rich region and linear polysaccharide of endocan are necessary for the protein to exert its biological functions. Elevated plasma endocan levels reflect endothelial activation and dysfunction. In addition, endocan participates in complex inflammatory responses and proliferative processes. Here, we reviewed current research on endocan, elaborated the protein’s structure and biological functions, and speculated on its possible clinical value in nervous system diseases. We conclude that endocan may be a glycoprotein that plays an important role in neurological disorders.","PeriodicalId":12450,"journal":{"name":"Frontiers in Aging Neuroscience","volume":"1 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142214243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-12eCollection Date: 2024-01-01DOI: 10.3389/fnagi.2024.1412735
Tao-Ran Li, Bai-Le Li, Xin-Ran Xu, Jin Zhong, Tai-Shan Wang, Feng-Qi Liu
Background: The relationship between white matter hyperintensities (WMH) and the core features of Alzheimer's disease (AD) remains controversial. Further, due to the prevalence of co-pathologies, the precise role of WMH in cognition and neurodegeneration also remains uncertain.
Methods: Herein, we analyzed 1803 participants with available WMH volume data, extracted from the ADNI database, including 756 cognitively normal controls, 783 patients with mild cognitive impairment (MCI), and 264 patients with dementia. Participants were grouped according to cerebrospinal fluid (CSF) pathology (A/T profile) severity. Linear regression analysis was applied to evaluate the factors associated with WMH volume. Modeled by linear mixed-effects, the increase rates (Δ) of the WMH volume, cognition, and typical neurodegenerative markers were assessed. The predictive effectiveness of WMH volume was subsequently tested using Cox regression analysis, and the relationship between WMH/ΔWMH and other indicators such as cognition was explored through linear regression analyses. Furthermore, we explored the interrelationship among amyloid-β deposition, cognition, and WMH using mediation analysis.
Results: Higher WMH volume was associated with older age, lower CSF amyloid-β levels, hypertension, and smoking history (all p ≤ 0.001), as well as cognitive status (MCI, p < 0.001; dementia, p = 0.008), but not with CSF tau levels. These results were further verified in any clinical stage, except hypertension and smoking history in the dementia stage. Although WMH could not predict dementia conversion, its increased levels at baseline were associated with a worse cognitive performance and a more rapid memory decline. Longitudinal analyses showed that baseline dementia and positive amyloid-β status were associated with a greater accrual of WMH volume, and a higher ΔWMH was also correlated with a faster cognitive decline. In contrast, except entorhinal cortex thickness, the WMH volume was not found to be associated with any other neurodegenerative markers. To a lesser extent, WMH mediates the relationship between amyloid-β and cognition.
Conclusion: WMH are non-specific lesions that are associated with amyloid-β deposition, cognitive status, and a variety of vascular risk factors. Despite evidence indicating only a weak relationship with neurodegeneration, early intervention to reduce WMH lesions remains a high priority for preserving cognitive function in the elderly.
{"title":"Association of white matter hyperintensities with cognitive decline and neurodegeneration.","authors":"Tao-Ran Li, Bai-Le Li, Xin-Ran Xu, Jin Zhong, Tai-Shan Wang, Feng-Qi Liu","doi":"10.3389/fnagi.2024.1412735","DOIUrl":"https://doi.org/10.3389/fnagi.2024.1412735","url":null,"abstract":"<p><strong>Background: </strong>The relationship between white matter hyperintensities (WMH) and the core features of Alzheimer's disease (AD) remains controversial. Further, due to the prevalence of co-pathologies, the precise role of WMH in cognition and neurodegeneration also remains uncertain.</p><p><strong>Methods: </strong>Herein, we analyzed 1803 participants with available WMH volume data, extracted from the ADNI database, including 756 cognitively normal controls, 783 patients with mild cognitive impairment (MCI), and 264 patients with dementia. Participants were grouped according to cerebrospinal fluid (CSF) pathology (A/T profile) severity. Linear regression analysis was applied to evaluate the factors associated with WMH volume. Modeled by linear mixed-effects, the increase rates (Δ) of the WMH volume, cognition, and typical neurodegenerative markers were assessed. The predictive effectiveness of WMH volume was subsequently tested using Cox regression analysis, and the relationship between WMH/ΔWMH and other indicators such as cognition was explored through linear regression analyses. Furthermore, we explored the interrelationship among amyloid-β deposition, cognition, and WMH using mediation analysis.</p><p><strong>Results: </strong>Higher WMH volume was associated with older age, lower CSF amyloid-β levels, hypertension, and smoking history (all <i>p</i> ≤ 0.001), as well as cognitive status (MCI, <i>p</i> < 0.001; dementia, <i>p</i> = 0.008), but not with CSF tau levels. These results were further verified in any clinical stage, except hypertension and smoking history in the dementia stage. Although WMH could not predict dementia conversion, its increased levels at baseline were associated with a worse cognitive performance and a more rapid memory decline. Longitudinal analyses showed that baseline dementia and positive amyloid-β status were associated with a greater accrual of WMH volume, and a higher ΔWMH was also correlated with a faster cognitive decline. In contrast, except entorhinal cortex thickness, the WMH volume was not found to be associated with any other neurodegenerative markers. To a lesser extent, WMH mediates the relationship between amyloid-β and cognition.</p><p><strong>Conclusion: </strong>WMH are non-specific lesions that are associated with amyloid-β deposition, cognitive status, and a variety of vascular risk factors. Despite evidence indicating only a weak relationship with neurodegeneration, early intervention to reduce WMH lesions remains a high priority for preserving cognitive function in the elderly.</p>","PeriodicalId":12450,"journal":{"name":"Frontiers in Aging Neuroscience","volume":"16 ","pages":"1412735"},"PeriodicalIF":4.1,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11425965/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142344650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BackgroundObservational studies have suggested that plasma lipidome play a pivotal role in the occurrence of Parkinson’s disease (PD). However, it remains unknown which lipids among plasma lipidome affect PD and how they exert their influence. Clarity is lacking regarding the causal relationship between plasma lipidome and PD, as well as whether circulating inflammatory proteins serve as mediators.MethodsSingle nucleotide polymorphisms (SNPs) significantly associated with 179 plasma lipidome were selected as instrumental variables to assess their causal impact on PD. PD data, serving as the outcome, were sourced from the International Parkinson’s Disease Genomics Consortium, which boasts the largest sample size to date. The inverse variance weighted (IVW), Weighted median method, MR-Egger method, Simple mode method, Weighted mode method and MR-PRESSO were employed to evaluate the influence of the 179 plasma lipidome on PD. Heterogeneity, pleiotropy tests, and reverse causality analyses were conducted accordingly. Additionally, we analyzed the causal relationship between 91 circulating inflammatory proteins and PD, exploring whether these proteins serve as mediators in the pathway from plasma lipidome to PD.ResultsAmong the 179 plasma lipidome, three were found to be associated with a reduced risk of PD: Phosphatidylcholine (14:0_18:2) (IVW, OR = 0.877; 95%CI, 0.787–0.978; <jats:italic>p</jats:italic> = 0.018), Phosphatidylcholine (16:0_16:1) levels (IVW, OR = 0.835; 95%CI, 0.717–0.973; <jats:italic>p</jats:italic> = 0.021), and Phosphatidylcholine (O-17:0_17:1) levels (IVW, OR = 0.854; 95%CI, 0.779–0.936; <jats:italic>p</jats:italic> = 0.001). Meanwhile, Sphingomyelin (d38:1) was linked to an increased risk of PD (IVW, OR = 1.095; 95%CI, 1.027–1.166; <jats:italic>p</jats:italic> = 0.005). Among the 91 circulating inflammatory proteins, three were associated with a lower PD risk: Fibroblast growth factor 21 levels (IVW, OR = 0.817; 95%CI, 0.674–0.990; <jats:italic>p</jats:italic> = 0.039), Transforming growth factor-alpha levels (IVW, OR = 0.825; 95%CI, 0.683–0.998; <jats:italic>p</jats:italic> = 0.048), and Tumor necrosis factor receptor superfamily member 9 levels (IVW, OR = 0.846; 95%CI, 0.744–0.963; <jats:italic>p</jats:italic> = 0.011). Two were associated with a higher risk of PD: Interleukin-17A levels (IVW, OR = 1.285; 95%CI, 1.051–1.571; <jats:italic>p</jats:italic> = 0.014) and TNF-beta levels (IVW, OR = 1.088; 95%CI, 1.010–1.171; <jats:italic>p</jats:italic> = 0.026). Additionally, a positive correlation was observed between Phosphatidylcholine (14:0_18:2) levels and Fibroblast growth factor 21 levels (IVW, OR = 1.125; 95%CI, 1.006–1.257; <jats:italic>p</jats:italic> = 0.038), suggesting that Fibroblast growth factor 21 levels may serve as a mediating factor in the pathway between Phosphatidylcholine (14.0_18.2) levels and PD. The mediation effect was estimated to be −0.024, accounting for approximately 18% of the total effect.Conclusio
{"title":"Plasma lipidome, circulating inflammatory proteins, and Parkinson’s disease: a Mendelian randomization study","authors":"Yidan Qin, Lin Wang, Jia Song, Wei Quan, Jing Xu, Jiajun Chen","doi":"10.3389/fnagi.2024.1424056","DOIUrl":"https://doi.org/10.3389/fnagi.2024.1424056","url":null,"abstract":"BackgroundObservational studies have suggested that plasma lipidome play a pivotal role in the occurrence of Parkinson’s disease (PD). However, it remains unknown which lipids among plasma lipidome affect PD and how they exert their influence. Clarity is lacking regarding the causal relationship between plasma lipidome and PD, as well as whether circulating inflammatory proteins serve as mediators.MethodsSingle nucleotide polymorphisms (SNPs) significantly associated with 179 plasma lipidome were selected as instrumental variables to assess their causal impact on PD. PD data, serving as the outcome, were sourced from the International Parkinson’s Disease Genomics Consortium, which boasts the largest sample size to date. The inverse variance weighted (IVW), Weighted median method, MR-Egger method, Simple mode method, Weighted mode method and MR-PRESSO were employed to evaluate the influence of the 179 plasma lipidome on PD. Heterogeneity, pleiotropy tests, and reverse causality analyses were conducted accordingly. Additionally, we analyzed the causal relationship between 91 circulating inflammatory proteins and PD, exploring whether these proteins serve as mediators in the pathway from plasma lipidome to PD.ResultsAmong the 179 plasma lipidome, three were found to be associated with a reduced risk of PD: Phosphatidylcholine (14:0_18:2) (IVW, OR = 0.877; 95%CI, 0.787–0.978; <jats:italic>p</jats:italic> = 0.018), Phosphatidylcholine (16:0_16:1) levels (IVW, OR = 0.835; 95%CI, 0.717–0.973; <jats:italic>p</jats:italic> = 0.021), and Phosphatidylcholine (O-17:0_17:1) levels (IVW, OR = 0.854; 95%CI, 0.779–0.936; <jats:italic>p</jats:italic> = 0.001). Meanwhile, Sphingomyelin (d38:1) was linked to an increased risk of PD (IVW, OR = 1.095; 95%CI, 1.027–1.166; <jats:italic>p</jats:italic> = 0.005). Among the 91 circulating inflammatory proteins, three were associated with a lower PD risk: Fibroblast growth factor 21 levels (IVW, OR = 0.817; 95%CI, 0.674–0.990; <jats:italic>p</jats:italic> = 0.039), Transforming growth factor-alpha levels (IVW, OR = 0.825; 95%CI, 0.683–0.998; <jats:italic>p</jats:italic> = 0.048), and Tumor necrosis factor receptor superfamily member 9 levels (IVW, OR = 0.846; 95%CI, 0.744–0.963; <jats:italic>p</jats:italic> = 0.011). Two were associated with a higher risk of PD: Interleukin-17A levels (IVW, OR = 1.285; 95%CI, 1.051–1.571; <jats:italic>p</jats:italic> = 0.014) and TNF-beta levels (IVW, OR = 1.088; 95%CI, 1.010–1.171; <jats:italic>p</jats:italic> = 0.026). Additionally, a positive correlation was observed between Phosphatidylcholine (14:0_18:2) levels and Fibroblast growth factor 21 levels (IVW, OR = 1.125; 95%CI, 1.006–1.257; <jats:italic>p</jats:italic> = 0.038), suggesting that Fibroblast growth factor 21 levels may serve as a mediating factor in the pathway between Phosphatidylcholine (14.0_18.2) levels and PD. The mediation effect was estimated to be −0.024, accounting for approximately 18% of the total effect.Conclusio","PeriodicalId":12450,"journal":{"name":"Frontiers in Aging Neuroscience","volume":"122 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142214244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-11DOI: 10.3389/fnagi.2024.1466089
Tingting Yi, Zhou Su, Jiyang Wang, Jinghuan Gan, Hao Wu, Zhihong Shi, Zhen Sun, Shuai Liu, Yong Ji
Background and aimsThe association between blood pressure (BP) and dementia in older adults remains unclear, prompting this study to investigate the relationship between various BP indicators and dementia in this population.MethodsA cross-sectional survey was conducted in 2019, including 3,599 participants aged 65 years or older. The basic demographic characteristics of participants were collected. BP measurements and neuropsychological assessments were performed. From the systolic BP (SBP) and diastolic BP (DBP) values, mean arterial pressure (MAP), pulse pressure (PP) and blood pressure index (BPI) were calculated. Generalized additive models and logistic regression models were used to analyze the association between BP indicators and dementia.ResultsGeneralized additive models identified a U-shaped relationship between DBP and dementia, which was more significant in males and people 70 years of age and older. The optimal DBP associated with the lowest dementia risk was 85 mmHg. Logistic regression models revealed that compared to the DBP subgroup (80–89 mmHg), participants in the DBP < 80 mmHg subgroup and the DBP ≥100 mmHg subgroup had OR for dementia of 1.611 (95% CI: 1. 252–2.073, P < 0.001) and 1.423 (95% CI: 0.999–2.028, p = 0.050), respectively. A significant association was observed between BPI and dementia (OR:1.746 95% CI: 1.142–2.668, p = 0.010).ConclusionIn older adults, we found a U-shaped relationship between DBP and dementia, and a linear relationship between BPI and dementia. These results underscore the importance of considering DBP and BPI in BP management strategies for older adults to potentially prevent or delay dementia onset.
{"title":"Association between blood pressure and dementia in older adults: a cross-sectional study from China","authors":"Tingting Yi, Zhou Su, Jiyang Wang, Jinghuan Gan, Hao Wu, Zhihong Shi, Zhen Sun, Shuai Liu, Yong Ji","doi":"10.3389/fnagi.2024.1466089","DOIUrl":"https://doi.org/10.3389/fnagi.2024.1466089","url":null,"abstract":"Background and aimsThe association between blood pressure (BP) and dementia in older adults remains unclear, prompting this study to investigate the relationship between various BP indicators and dementia in this population.MethodsA cross-sectional survey was conducted in 2019, including 3,599 participants aged 65 years or older. The basic demographic characteristics of participants were collected. BP measurements and neuropsychological assessments were performed. From the systolic BP (SBP) and diastolic BP (DBP) values, mean arterial pressure (MAP), pulse pressure (PP) and blood pressure index (BPI) were calculated. Generalized additive models and logistic regression models were used to analyze the association between BP indicators and dementia.ResultsGeneralized additive models identified a U-shaped relationship between DBP and dementia, which was more significant in males and people 70 years of age and older. The optimal DBP associated with the lowest dementia risk was 85 mmHg. Logistic regression models revealed that compared to the DBP subgroup (80–89 mmHg), participants in the DBP &lt; 80 mmHg subgroup and the DBP ≥100 mmHg subgroup had OR for dementia of 1.611 (95% CI: 1. 252–2.073, <jats:italic>P</jats:italic> &lt; 0.001) and 1.423 (95% CI: 0.999–2.028, <jats:italic>p</jats:italic> = 0.050), respectively. A significant association was observed between BPI and dementia (OR:1.746 95% CI: 1.142–2.668, <jats:italic>p</jats:italic> = 0.010).ConclusionIn older adults, we found a U-shaped relationship between DBP and dementia, and a linear relationship between BPI and dementia. These results underscore the importance of considering DBP and BPI in BP management strategies for older adults to potentially prevent or delay dementia onset.","PeriodicalId":12450,"journal":{"name":"Frontiers in Aging Neuroscience","volume":"72 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142214255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-10DOI: 10.3389/fnagi.2024.1431277
Zhao HongFei, Zhang Li, Li Liang, Guo Wan Ru, Huang Lan Yi, Wang Zhen
AimTo identify optimally therapeutic exercise interventions for improving motor ability among patients with Parkinson’s disease (PD), we conducted a network meta-analysis (NMA) of randomized controlled trials comparing different exercise regimens.MethodsRelevant RCTs were retrieved by searching PubMed, Embase, Cochrane, Web of Science, CINAHL, CBM, China National Knowledge Infrastructure (CNKI), Wan fang, VIP, and other databases from inception to July 9, 2023 is available in English as the primary language. Exercise outcomes as measured by Movement Disorder Society- Unified Parkinson’s Disease Rating Scale Part III (MDS-UPDRS-III) score change were evaluated and ranked using STATA software version 18.0. All included studies were assessed for methodological quality using the Cochrane Risk of Bias tool.ResultsThe final NMA included 71 studies involving 3,732 participants, 87 intervention experiments, and 27distinct interventions. Although most exercise interventions showed some efficacy (reducing MDS-UPDRS-III score), cumulative ranking probability surface (SUCRA) values indicated that the best exercise interventions for motor function improvement were archery (95.6%), riding a bicycle (80.9%), and binary rhythm dance (80.8%).ConclusionAn exercise intervention comprising archery, cycling, and(or) binary rhythm dance may yield superior improvements in motor function among patients with Parkinson’s disease.
方法通过检索PubMed、Embase、Cochrane、Web of Science、CINAHL、CBM、中国国家知识基础设施（CNKI）、万方、VIP等数据库，以英语为主要语言，检索了从开始到2023年7月9日的相关RCT。通过运动障碍协会-帕金森病统一评分量表第三部分（MDS-UPDRS-III）的评分变化来衡量运动效果，并使用 STATA 软件 18.0 版进行评估和排序。所有纳入的研究均使用 Cochrane 偏倚风险工具进行了方法学质量评估。结果最终的 NMA 纳入了 71 项研究，涉及 3732 名参与者、87 项干预实验和 27 种不同的干预措施。尽管大多数运动干预显示出一定的疗效（降低 MDS-UPDRS-III 评分），但累积排序概率面（SUCRA）值显示，运动功能改善效果最好的运动干预是射箭（95.6%）、骑自行车（80.9%）和二元韵律舞蹈（80.8%）。
{"title":"Current interventional model for movement in Parkinson’s disease: network meta-analysis based on the improvement of motor ability","authors":"Zhao HongFei, Zhang Li, Li Liang, Guo Wan Ru, Huang Lan Yi, Wang Zhen","doi":"10.3389/fnagi.2024.1431277","DOIUrl":"https://doi.org/10.3389/fnagi.2024.1431277","url":null,"abstract":"AimTo identify optimally therapeutic exercise interventions for improving motor ability among patients with Parkinson’s disease (PD), we conducted a network meta-analysis (NMA) of randomized controlled trials comparing different exercise regimens.MethodsRelevant RCTs were retrieved by searching PubMed, Embase, Cochrane, Web of Science, CINAHL, CBM, China National Knowledge Infrastructure (CNKI), Wan fang, VIP, and other databases from inception to July 9, 2023 is available in English as the primary language. Exercise outcomes as measured by Movement Disorder Society- Unified Parkinson’s Disease Rating Scale Part III (MDS-UPDRS-III) score change were evaluated and ranked using STATA software version 18.0. All included studies were assessed for methodological quality using the Cochrane Risk of Bias tool.ResultsThe final NMA included 71 studies involving 3,732 participants, 87 intervention experiments, and 27distinct interventions. Although most exercise interventions showed some efficacy (reducing MDS-UPDRS-III score), cumulative ranking probability surface (SUCRA) values indicated that the best exercise interventions for motor function improvement were archery (95.6%), riding a bicycle (80.9%), and binary rhythm dance (80.8%).ConclusionAn exercise intervention comprising archery, cycling, and(or) binary rhythm dance may yield superior improvements in motor function among patients with Parkinson’s disease.","PeriodicalId":12450,"journal":{"name":"Frontiers in Aging Neuroscience","volume":"59 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142214254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-09DOI: 10.3389/fnagi.2024.1444998
Ha Eun Kim, Bori R. Kim, Sang Hi Hong, Seung Yeon Song, Jee Hyang Jeong, Geon Ha Kim
ObjectiveCognitive decline is often considered an inevitable aspect of aging; however, recent research has identified a subset of older adults known as “superagers” who maintain cognitive abilities comparable to those of younger individuals. Investigating the neurobiological characteristics associated with superior cognitive function in superagers is essential for understanding “successful aging.” Evidence suggests that the gut microbiome plays a key role in brain function, forming a bidirectional communication network known as the microbiome-gut-brain axis. Alterations in the gut microbiome have been linked to cognitive aging markers such as oxidative stress and inflammation. This study aims to investigate the unique patterns of the gut microbiome in superagers and to develop machine learning-based predictive models to differentiate superagers from typical agers.MethodsWe recruited 161 cognitively unimpaired, community-dwelling volunteers aged 60 years or from dementia prevention centers in Seoul, South Korea. After applying inclusion and exclusion criteria, 115 participants were included in the study. Following the removal of microbiome data outliers, 102 participants, comprising 57 superagers and 45 typical agers, were finally analyzed. Superagers were defined based on memory performance at or above average normative values of middle-aged adults. Gut microbiome data were collected from stool samples, and microbial DNA was extracted and sequenced. Relative abundances of bacterial genera were used as features for model development. We employed the LightGBM algorithm to build predictive models and utilized SHAP analysis for feature importance and interpretability.ResultsThe predictive model achieved an AUC of 0.832 and accuracy of 0.764 in the training dataset, and an AUC of 0.861 and accuracy of 0.762 in the test dataset. Significant microbiome features for distinguishing superagers included Alistipes, PAC001137_g, PAC001138_g, Leuconostoc, and PAC001115_g. SHAP analysis revealed that higher abundances of certain genera, such as PAC001138_g and PAC001115_g, positively influenced the likelihood of being classified as superagers.ConclusionOur findings demonstrate the machine learning-based predictive models using gut-microbiome features can differentiate superagers from typical agers with a reasonable performance.
{"title":"Predicting superagers: a machine learning approach utilizing gut microbiome features","authors":"Ha Eun Kim, Bori R. Kim, Sang Hi Hong, Seung Yeon Song, Jee Hyang Jeong, Geon Ha Kim","doi":"10.3389/fnagi.2024.1444998","DOIUrl":"https://doi.org/10.3389/fnagi.2024.1444998","url":null,"abstract":"ObjectiveCognitive decline is often considered an inevitable aspect of aging; however, recent research has identified a subset of older adults known as “superagers” who maintain cognitive abilities comparable to those of younger individuals. Investigating the neurobiological characteristics associated with superior cognitive function in superagers is essential for understanding “successful aging.” Evidence suggests that the gut microbiome plays a key role in brain function, forming a bidirectional communication network known as the microbiome-gut-brain axis. Alterations in the gut microbiome have been linked to cognitive aging markers such as oxidative stress and inflammation. This study aims to investigate the unique patterns of the gut microbiome in superagers and to develop machine learning-based predictive models to differentiate superagers from typical agers.MethodsWe recruited 161 cognitively unimpaired, community-dwelling volunteers aged 60 years or from dementia prevention centers in Seoul, South Korea. After applying inclusion and exclusion criteria, 115 participants were included in the study. Following the removal of microbiome data outliers, 102 participants, comprising 57 superagers and 45 typical agers, were finally analyzed. Superagers were defined based on memory performance at or above average normative values of middle-aged adults. Gut microbiome data were collected from stool samples, and microbial DNA was extracted and sequenced. Relative abundances of bacterial genera were used as features for model development. We employed the LightGBM algorithm to build predictive models and utilized SHAP analysis for feature importance and interpretability.ResultsThe predictive model achieved an AUC of 0.832 and accuracy of 0.764 in the training dataset, and an AUC of 0.861 and accuracy of 0.762 in the test dataset. Significant microbiome features for distinguishing superagers included Alistipes, PAC001137_g, PAC001138_g, Leuconostoc, and PAC001115_g. SHAP analysis revealed that higher abundances of certain genera, such as PAC001138_g and PAC001115_g, positively influenced the likelihood of being classified as superagers.ConclusionOur findings demonstrate the machine learning-based predictive models using gut-microbiome features can differentiate superagers from typical agers with a reasonable performance.","PeriodicalId":12450,"journal":{"name":"Frontiers in Aging Neuroscience","volume":"42 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142214256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-05DOI: 10.3389/fnagi.2024.1458542
Jianlong Zhou, Yadi Li, Lv Zhu, Rensong Yue
BackgroundAs the population ages, the occurrence of cognitive decline and dementia is continuously increasing. Frailty is a prevalent problem among older adults. Epidemiologic studies have shown a comorbidity between frailty and cognitive impairment. However, their relationship remains unclear. The frailty index is an important indicator for measuring frailty. This study aims to investigate the relationship between frailty index and cognitive dysfunction in older adults aged 60 years and older in the United States from the 2011–2014 National Health and Nutrition Examination Survey (NHANES).MethodsCommunity-dwelling older adults aged 60 years or older from 2011 to 2014 were extracted from the NHANES database. The frailty index was calculated using the formula: frailty index = total number of deficits present/total number of deficits measured. The Animal Fluency (AF), the Digit Symbol Substitution Test (DSST), the Consortium to Establish a Registry for Alzheimer’s disease Delayed Recall (CERAD-DR), and Word Learning (CERAD-WL) were used to evaluate cognitive dysfunction. Firstly, weighted logistic regression analysis was used to explore the relationship between frailty index and cognitive dysfunction. Secondly, the influence of covariates on the frailty index was evaluated by subgroup analysis and interaction. Finally, the non-linear relationship is discussed by using the restricted cubic spline regression model.ResultsOur study included a total of 2,574 patients, weighted logistic regression analysis, after adjusting for all covariates, showed that the frailty index was associated with every test score. The interaction showed that covariates had no significant effect on this association in AF. The association between the frailty index and AF in the restricted cubic spline regression model is non-linear. As the frailty index increased, the risk of AF reduction increased, suggesting a higher risk of cognitive dysfunction.ConclusionIn general, a high frailty index appears to be associated with an increased risk of cognitive dysfunction in the elderly. Consequently, protecting against cognitive decline necessitates making geriatric frailty prevention and treatment top priorities.
{"title":"Association between frailty index and cognitive dysfunction in older adults: insights from the 2011–2014 NHANES data","authors":"Jianlong Zhou, Yadi Li, Lv Zhu, Rensong Yue","doi":"10.3389/fnagi.2024.1458542","DOIUrl":"https://doi.org/10.3389/fnagi.2024.1458542","url":null,"abstract":"BackgroundAs the population ages, the occurrence of cognitive decline and dementia is continuously increasing. Frailty is a prevalent problem among older adults. Epidemiologic studies have shown a comorbidity between frailty and cognitive impairment. However, their relationship remains unclear. The frailty index is an important indicator for measuring frailty. This study aims to investigate the relationship between frailty index and cognitive dysfunction in older adults aged 60 years and older in the United States from the 2011–2014 National Health and Nutrition Examination Survey (NHANES).MethodsCommunity-dwelling older adults aged 60 years or older from 2011 to 2014 were extracted from the NHANES database. The frailty index was calculated using the formula: frailty index = total number of deficits present/total number of deficits measured. The Animal Fluency (AF), the Digit Symbol Substitution Test (DSST), the Consortium to Establish a Registry for Alzheimer’s disease Delayed Recall (CERAD-DR), and Word Learning (CERAD-WL) were used to evaluate cognitive dysfunction. Firstly, weighted logistic regression analysis was used to explore the relationship between frailty index and cognitive dysfunction. Secondly, the influence of covariates on the frailty index was evaluated by subgroup analysis and interaction. Finally, the non-linear relationship is discussed by using the restricted cubic spline regression model.ResultsOur study included a total of 2,574 patients, weighted logistic regression analysis, after adjusting for all covariates, showed that the frailty index was associated with every test score. The interaction showed that covariates had no significant effect on this association in AF. The association between the frailty index and AF in the restricted cubic spline regression model is non-linear. As the frailty index increased, the risk of AF reduction increased, suggesting a higher risk of cognitive dysfunction.ConclusionIn general, a high frailty index appears to be associated with an increased risk of cognitive dysfunction in the elderly. Consequently, protecting against cognitive decline necessitates making geriatric frailty prevention and treatment top priorities.","PeriodicalId":12450,"journal":{"name":"Frontiers in Aging Neuroscience","volume":"10 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142214257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-04DOI: 10.3389/fnagi.2024.1388290
Yanqing Zhao, Li Huang, Wentao Li
ObjectiveThis study points to probing the inclination and mapping knowledge domain of acupuncture for Parkinson’s disease through bibliometrics.MethodsA search was conducted on 1 February 2024 using the Web of Science to identify papers published on acupuncture for Parkinson’s disease. The analysis included scientific research, countries, organizations, authors/cited authors, keywords, journals, and cited references. Bibliometric data were analyzed using VOSviewer software, CiteSpace, GraphPad Prism, and Scimago Graphica. The studies on acupuncture for Parkinson’s disease were visualized as a network map according to the publication year.ResultsThe cumulative publication trend on acupuncture for Parkinson’s disease is increasing year by year. China is the leading contributor in this field. International collaboration is predominantly concentrated in Europe, while institutional collaboration is chiefly limited to Chinese universities specializing in traditional Chinese medicine. Park HJ is the most prolific author, with “Movement Disorders” being the journal with the most publications. “Brain Research” is identified as a key journal, reflecting a focus on neuroscience. Kim SN is the most cited author, while Eisenberg DM is a prominent author in this field. Research topics such as mouse models, systematic reviews, and non-motor symptoms are frequently explored, with messenger RNA of substantia nigra emerging as a notable keyword in this field. Choi YG’s 2009 paper, published in the Neuroscience Letters journal, is a critical reference in this field. Key papers include Eisenberg DM’s 1998 study on randomized trials of acupuncture for non-motor symptoms of PD, as well as research focusing on the neuroinflammatory regulatory mechanisms of acupuncture for PD.ConclusionThe bibliometric analysis offers an exhaustive generality of the advancement and worldwide trends in acupuncture treatments for Parkinson’s disease, shedding light on potential avenues for prospective research.
{"title":"Mapping knowledge domain of acupuncture for Parkinson’s disease: a bibliometric and visual analysis","authors":"Yanqing Zhao, Li Huang, Wentao Li","doi":"10.3389/fnagi.2024.1388290","DOIUrl":"https://doi.org/10.3389/fnagi.2024.1388290","url":null,"abstract":"ObjectiveThis study points to probing the inclination and mapping knowledge domain of acupuncture for Parkinson’s disease through bibliometrics.MethodsA search was conducted on 1 February 2024 using the Web of Science to identify papers published on acupuncture for Parkinson’s disease. The analysis included scientific research, countries, organizations, authors/cited authors, keywords, journals, and cited references. Bibliometric data were analyzed using VOSviewer software, CiteSpace, GraphPad Prism, and Scimago Graphica. The studies on acupuncture for Parkinson’s disease were visualized as a network map according to the publication year.ResultsThe cumulative publication trend on acupuncture for Parkinson’s disease is increasing year by year. China is the leading contributor in this field. International collaboration is predominantly concentrated in Europe, while institutional collaboration is chiefly limited to Chinese universities specializing in traditional Chinese medicine. Park HJ is the most prolific author, with “Movement Disorders” being the journal with the most publications. “Brain Research” is identified as a key journal, reflecting a focus on neuroscience. Kim SN is the most cited author, while Eisenberg DM is a prominent author in this field. Research topics such as mouse models, systematic reviews, and non-motor symptoms are frequently explored, with messenger RNA of substantia nigra emerging as a notable keyword in this field. Choi YG’s 2009 paper, published in the <jats:italic>Neuroscience Letters</jats:italic> journal, is a critical reference in this field. Key papers include Eisenberg DM’s 1998 study on randomized trials of acupuncture for non-motor symptoms of PD, as well as research focusing on the neuroinflammatory regulatory mechanisms of acupuncture for PD.ConclusionThe bibliometric analysis offers an exhaustive generality of the advancement and worldwide trends in acupuncture treatments for Parkinson’s disease, shedding light on potential avenues for prospective research.","PeriodicalId":12450,"journal":{"name":"Frontiers in Aging Neuroscience","volume":"11 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142214260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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