Frontiers in Aging Neuroscience最新文献

{"title":"Correspondence between white matter hyperintensities and regional grey matter volumes in Alzheimer's disease.","authors":"Fangyuan Yi, Jirui Wang, Meiqing Lin, Baizhu Li, Shiyu Han, Shan Wang, Yingbin Jin, Ning Hu, Yutong Chen, Xiuli Shang","doi":"10.3389/fnagi.2024.1429098","DOIUrl":"10.3389/fnagi.2024.1429098","url":null,"abstract":"<p><strong>Objective: </strong>White matter hyperintensities (WMH) are the most common neuroimaging manifestation of cerebral small vessel disease, and is frequently observed in Alzheimer's disease (AD). This study aimed to investigate the relationship between WMH and cognition and to verify the mediation of grey matter atrophy in this relationship.</p><p><strong>Methods: </strong>The diffusion tensor imaging (DTI) technique analyses white matter fiber tract to assess white matter integrity. Voxel-based morphometry was applied to measure the grey matter volume (GMV). A linear regression model was applied to examine the associations between WMH and GMV, and mediation analyses was performed to determine the mediating role of regional GMV in the effect of WMH on cognitive function.</p><p><strong>Results: </strong>Compared to the HC group, AD group have 8 fiber tract fractional anisotropy (FA) decreased and 16 fiber tract mean diffusivity (MD) increased. Compared to AD without WMH, AD with high WMH had 9 fiber tracts FA decreased and 13 fiber tracts MD increased. High WMH volume was negatively correlated with GMV in the frontal-parietal region. Low WMH volume was also negatively correlated with GMV except for the three regions (right angular gyrus, right superior frontal gyrus and right middle/inferior parietal gyrus), where GMV was positively correlated. Mediation analysis showed that the association between WMH and executive function or episodic memory were mediated by GMV in the frontal-parietal region.</p><p><strong>Conclusion: </strong>Damage to white matter integrity was more severe in AD with WMH. Differential changes in DTI metrics may be caused by progressive myelin and axonal damage. There was a negative correlation between WMH and grey matter atrophy in frontal-parietal regions in a volume-dependent manner. This study indicates the correspondence between WMH volume and GMV in cognition, and GMV being a key modulator between WMH and cognition in AD. This result will contribute to understanding the progression of the disease process and applying targeted therapeutic intervention in the earlier stage to delay neurodegenerative changes in frontal-parietal regions to achieve better treatment outcomes and affordability.</p>","PeriodicalId":12450,"journal":{"name":"Frontiers in Aging Neuroscience","volume":"16 ","pages":"1429098"},"PeriodicalIF":4.1,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439820/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142344651","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}

{"title":"Subthreshold amyloid deposition, cerebral small vessel disease, and functional brain network disruption in delayed cognitive decline after stroke.","authors":"Jae-Sung Lim, Jae-Joong Lee, Geon Ha Kim, Hang-Rai Kim, Dong Woo Shin, Keon-Joo Lee, Min Jae Baek, Eunvin Ko, Beom Joon Kim, SangYun Kim, Wi-Sun Ryu, Jinyong Chung, Dong-Eog Kim, Philip B Gorelick, Choong-Wan Woo, Hee-Joon Bae","doi":"10.3389/fnagi.2024.1430408","DOIUrl":"10.3389/fnagi.2024.1430408","url":null,"abstract":"<p><strong>Background: </strong>Although its incidence is relatively low, delayed-onset post-stroke cognitive decline (PSCD) may offer valuable insights into the \"vascular contributions to cognitive impairment and dementia,\" particularly concerning the roles of vascular and neurodegenerative mechanisms. We postulated that the functional segregation observed during post-stroke compensation could be disrupted by underlying amyloid pathology or cerebral small vessel disease (cSVD), leading to delayed-onset PSCD.</p><p><strong>Methods: </strong>Using a prospective stroke registry, we identified patients who displayed normal cognitive function at baseline evaluation within a year post-stroke and received at least one subsequent assessment. Patients suspected of pre-stroke cognitive decline were excluded. Decliners [defined by a decrease of ≥3 Mini-Mental State Examination (MMSE) points annually or an absolute drop of ≥5 points between evaluations, confirmed with detailed neuropsychological tests] were compared with age- and stroke severity-matched non-decliners. Index-stroke MRI, resting-state functional MRI, and 18F-florbetaben PET were used to identify cSVD, functional network attributes, and amyloid deposits, respectively. PET data from age-, sex-, education-, and apolipoprotein E-matched stroke-free controls within a community-dwelling cohort were used to benchmark amyloid deposition.</p><p><strong>Results: </strong>Among 208 eligible patients, 11 decliners and 10 matched non-decliners were identified over an average follow-up of 5.7 years. No significant differences in cSVD markers were noted between the groups, except for white matter hyperintensities (WMHs), which were strongly linked with MMSE scores among decliners (rho = -0.85, <i>p</i> < 0.01). Only one decliner was amyloid-positive, yet subthreshold PET standardized uptake value ratios (SUVR) in amyloid-negative decliners inversely correlated with final MMSE scores (rho = -0.67, <i>p</i> = 0.04). Decliners exhibited disrupted modular structures and more intermingled canonical networks compared to non-decliners. Notably, the somato-motor network's system segregation corresponded with the decliners' final MMSE (rho = 0.67, <i>p</i> = 0.03) and was associated with WMH volume and amyloid SUVR.</p><p><strong>Conclusion: </strong>Disruptions in modular structures, system segregation, and inter-network communication in the brain may be the pathophysiological underpinnings of delayed-onset PSCD. WMHs and subthreshold amyloid deposition could contribute to these disruptions in functional brain networks. Given the limited number of patients and potential residual confounding, our results should be considered hypothesis-generating and need replication in larger cohorts in the future.</p>","PeriodicalId":12450,"journal":{"name":"Frontiers in Aging Neuroscience","volume":"16 ","pages":"1430408"},"PeriodicalIF":4.1,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439663/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142344652","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}

{"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 &lt;jats:italic&gt;R&lt;/jats:italic&gt;&lt;jats:sup&gt;2&lt;/jats:sup&gt; 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}

{"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}

{"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}

{"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}

{"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; &lt;jats:italic&gt;p&lt;/jats:italic&gt; = 0.018), Phosphatidylcholine (16:0_16:1) levels (IVW, OR = 0.835; 95%CI, 0.717–0.973; &lt;jats:italic&gt;p&lt;/jats:italic&gt; = 0.021), and Phosphatidylcholine (O-17:0_17:1) levels (IVW, OR = 0.854; 95%CI, 0.779–0.936; &lt;jats:italic&gt;p&lt;/jats:italic&gt; = 0.001). Meanwhile, Sphingomyelin (d38:1) was linked to an increased risk of PD (IVW, OR = 1.095; 95%CI, 1.027–1.166; &lt;jats:italic&gt;p&lt;/jats:italic&gt; = 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; &lt;jats:italic&gt;p&lt;/jats:italic&gt; = 0.039), Transforming growth factor-alpha levels (IVW, OR = 0.825; 95%CI, 0.683–0.998; &lt;jats:italic&gt;p&lt;/jats:italic&gt; = 0.048), and Tumor necrosis factor receptor superfamily member 9 levels (IVW, OR = 0.846; 95%CI, 0.744–0.963; &lt;jats:italic&gt;p&lt;/jats:italic&gt; = 0.011). Two were associated with a higher risk of PD: Interleukin-17A levels (IVW, OR = 1.285; 95%CI, 1.051–1.571; &lt;jats:italic&gt;p&lt;/jats:italic&gt; = 0.014) and TNF-beta levels (IVW, OR = 1.088; 95%CI, 1.010–1.171; &lt;jats:italic&gt;p&lt;/jats:italic&gt; = 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; &lt;jats:italic&gt;p&lt;/jats:italic&gt; = 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}

{"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 &amp;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> &amp;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}

{"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}

{"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}