The Journal of Prevention of Alzheimer's Disease最新文献

{"title":"Treatments for Alzheimer's and the declaration of Helsinki.","authors":"Timothy Daly, Andi Olluri, Markku Kurkinen","doi":"10.1016/j.tjpad.2025.100260","DOIUrl":"10.1016/j.tjpad.2025.100260","url":null,"abstract":"","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100260"},"PeriodicalIF":7.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12413695/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144529620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polyunsaturated fatty acids, APOE genotypes, and dementia incidence and mortality among hypertensive adults.","authors":"Yubo Zhang, Jindi Li, Shaohui Liu, Quanhong Chen, Xuexiu Wang, Sisi He, Yadong Wei, Yunfeng Zou, Yunan Xu, Lijun Wang, Hao Chen","doi":"10.1016/j.tjpad.2025.100297","DOIUrl":"10.1016/j.tjpad.2025.100297","url":null,"abstract":"<p><strong>Background: </strong>Individuals with hypertension have an elevated risk of dementia. The potential protective effects of dietary polyunsaturated fatty acids (PUFAs) against dementia remain unclear. In this study, we investigate associations between blood PUFA levels and dementia outcomes, while considering the genetic predisposition among hypertensive adults.</p><p><strong>Methods: </strong>We employed data from UK Biobank and a prospective cohort of 123,235 hypertensive participants aged 40-69 years were included for the analysis (2006-2022). Cox proportional hazards models adjusting for covariates were applied to assess the associations of blood levels of docosahexaenoic acid (DHA), N3FA, N6FA, linoleic acid (LA), total PUFA, and the N6FA/N3FA ratio with incident dementia, dementia mortality, and all-cause mortality. The analyses were also stratified by polygenic risk scores (PRS) or APOE genotypes.</p><p><strong>Results: </strong>Higher levels of DHA (HR 0.41, 95 % CI 0.27-0.62), N3FA, LA, N6FA, and total PUFA were associated with significantly reduced dementia incidence (P < 0.001). In contrast, a higher N6FA/N3FA ratio was linked to increased dementia risk. Similar trends were observed for mortality. APOE genotypes, rather than PRS, modified PUFA-dementia associations: individuals with low-to-moderate APOE risk showed greater protective effects of high PUFA levels compared to those with high-risk genotypes.</p><p><strong>Conclusions: </strong>Among hypertensive adults, higher PUFA levels are associated with reduced risks of dementia and mortality. An imbalanced N6FA/N3FA ratio increases risk, while APOE genotypes significantly modify PUFA-related dementia outcomes.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100297"},"PeriodicalIF":7.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12413715/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144691623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Causal relationship and mediating role between depression and cognitive performance.","authors":"Xinyu Hao, Fuyang Cao, Ziyao Xu, Shaohua You, Tianyue Mi, Lei Wang, Yongxin Guo, Zhuoning Zhang, Jiangbei Cao, Jingsheng Lou, Yanhong Liu, Xianyang Chen, Zhikang Zhou, Weidong Mi, Li Tong","doi":"10.1016/j.tjpad.2025.100196","DOIUrl":"10.1016/j.tjpad.2025.100196","url":null,"abstract":"<p><strong>Background: </strong>Recent studies have increasingly emphasized the robust correlation between depression and cognitive function. However, it remains unclear whether this relationship is causal or merely coincidental. To address this uncertainty, we conducted two-sample bidirectional Mendelian randomization (MR) analyses to investigate the connection between depression and cognitive performance.</p><p><strong>Methods: </strong>We sourced genome-wide association study (GWAS) data for depression (N_SNPs=21,306,230) from the FinnGen (R10) and for cognitive performance (N_SNPs=10,049,954) from the IEU GWAS database. Causal effects employed methodologies such as Inverse variance weighted (IVW), weighted median, MR Egger, simple mode and weighted mode. Two-step analysis determined the contribution of the mediator variable to the outcomes. To determine stability and reliability, sensitivity analyses were performed that included an assessment of heterogeneity, horizontal pleiotropy, and the leave-one-out techniques.</p><p><strong>Results: </strong>This MR analysis identified 8 independent significant SNPs associated with depression and 81 SNPs linked to cognitive performance. Our findings revealed that depression increases the risk of developing deteriorating cognitive performance (IVW β, -0.11; 95 % confidence interval (CI), -0.18 - -0.05; P_IVW value= 5.97E-04). Conversely, cognitive performance decline could also predispose individuals to depression [odds ratio (OR)_IVW, 0.85; 95 % CI, 0.76 - 0.95; P_IVW value=0.004]. Multivariate MR analysis confirmed the robustness of this bidirectional association. A two-step MR mediation analysis indicated that the pathway from depression to cognitive performance is mediated by pain, with a mediation effect size of -0.022 and a mediation ratio of 28.95 %. The pathway from cognitive performance to depression is mediated by frailty, with a mediation effect value of -0.028, representing 22.40 % of the mediation proportion.</p><p><strong>Conclusion: </strong>A two-way causal relationship between depression and cognitive performance, with pain and frailty being mediating factors, respectively. Future research should prioritize mechanistic studies, targeted interventions, and personalized approaches to disentangle and mitigate the bidirectional effects of depression and cognitive performance.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100196"},"PeriodicalIF":7.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12413711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144049154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Psychosocial stressors and cognitive function: An analysis using data from the English longitudinal study of ageing.","authors":"Jiahao Li, Natalia Ortí-Casañ, Irem Bayraktaroglu, Giulia Mozzanica, Feng Zhang, Jocelien D A Olivier, Ulrich L M Eisel","doi":"10.1016/j.tjpad.2025.100232","DOIUrl":"10.1016/j.tjpad.2025.100232","url":null,"abstract":"<p><strong>Background: </strong>Growing evidence suggests that psychosocial stressors-such as financial strain, caregiving responsibilities, disability, and limiting long-term illnesses-may contribute to accelerated cognitive decline in older adults. However, the heterogeneity of stressor profiles and their distinct impact on specific cognitive domains remain poorly understood.</p><p><strong>Objective: </strong>To examine the associations between varying burdens of psychosocial stressors and cognitive function over a 10-year period using data from the English Longitudinal Study of Ageing (ELSA).</p><p><strong>Methods: </strong>We used longitudinal data from wave 4 (2008-2009) to wave 9 (2018-2019) of ELSA, comprising 10,893 participants aged ≥50 years at baseline who had valid measurements of psychosocial stressors and cognitive outcomes. Psychosocial stressors-financial strain, caregiving, disability, and limiting long-term illness-were assessed as binary indicators and summed into three categories (No Stressors, One Stressor, Multiple Stressors). Cognitive function was assessed using an overall global cognition score and scores of three specific domains: memory, executive function, and orientation. Baseline associations were examined via multiple linear regression, while linear mixed-effects models evaluated longitudinal trajectories of cognitive change. All models were progressively adjusted for demographic, lifestyle, and clinical covariates.</p><p><strong>Results: </strong>At baseline, participants reporting multiple stressors (18.2 % of the sample) had significantly lower global cognitive and executive function scores compared to those with no stressors (43.3 %). Over the 10-year follow-up, a higher stress burden predicted faster declines in global cognition, memory, and executive function. These associations remained robust after adjusting for sociodemographic characteristics, health behaviors, and chronic conditions. Random intercept and random slope models yielded consistent findings, indicating a dose-response relationship between stress burden and cognitive deterioration.</p><p><strong>Conclusion: </strong>Older adults experiencing multiple psychosocial stressors face an elevated risk of both lower initial cognitive function and accelerated decline over time. These findings underscore the importance of identifying and mitigating modifiable stressors-such as financial strain and caregiving demands-to potentially preserve cognitive health in later life. Interventions tailored to individuals with higher stress burdens may be especially beneficial in slowing cognitive deterioration.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100232"},"PeriodicalIF":7.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12413730/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144326859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting cognitive aging with curcumin supplementation: A systematic review and meta-analysis.","authors":"Lirong Yu, Na Li, Bin Li, Kaisy Xinhong Ye, Jiuyu Guo, Jiatong Shan, Luwen Cao, Mei Song, Yanyu Wang, Tih-Shih Lee, Andrea B Maier, Lei Feng","doi":"10.1016/j.tjpad.2025.100248","DOIUrl":"10.1016/j.tjpad.2025.100248","url":null,"abstract":"<p><strong>Background: </strong>Cognitive aging is a growing public health concern, and curcumin, a bioactive compound derived from turmeric, has been proposed as a potential intervention to support cognitive function due to its anti-inflammatory and antioxidant properties.</p><p><strong>Objectives: </strong>This systematic review and meta-analysis aimed to evaluate the effects of curcumin on cognitive outcomes related to aging.</p><p><strong>Methods: </strong>A comprehensive search of PubMed, Embase, Cochrane Library, Web of Science, and Scopus was conducted to identify studies published up to June 18, 2024, including both in vivo preclinical animal studies and randomized controlled trials (RCTs) assessing curcumin's effects on cognitive function. In vivo animal studies using Alzheimer's disease (AD) models and RCTs in human participants were included. Data were extracted and analyzed using meta-analytic techniques.</p><p><strong>Results: </strong>In preclinical in vivo murine studies (n = 25; total animals = 572), curcumin consistently improved both acquisition memory (SMD = -1.78, 95 % CI: -2.12 to -1.43) and retention memory (SMD = 2.36, 95 % CI: 1.72 to 3.00) in rodent models of AD. Ten human studies include 531 participants. Overall, curcumin showed no significant effect on global cognitive outcomes compared to placebo (SMD = 0.14, 95 % CI: -0.78 to 1.07). Subgroup analyses revealed significant improvements in working memory (SMD = 1.01, 95 % CI: 0.15 to 1.87) and processing speed (SMD = 0.37, 95 % CI: 0.07 to 0.67). The incidence of adverse events was higher in the curcumin group than in the control group.</p><p><strong>Conclusions: </strong>Preclinical in vivo evidence suggests curcumin enhances cognitive function in AD models. However, human studies show inconsistent findings with benefits limited to specific cognitive domains. Larger, well-designed randomized controlled trials are needed to establish curcumin's efficacy and safety in cognitive aging.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100248"},"PeriodicalIF":7.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12413726/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of modified donanemab titration on amyloid-related imaging abnormalities with edema/effusions and amyloid reduction: 18-month results from TRAILBLAZER-ALZ 6.","authors":"Hong Wang, Emel Serap Monkul Nery, Paul Ardayfio, Rashna Khanna, Diana Otero Svaldi, Sergey Shcherbinin, Wen Xu, Scott W Andersen, Paula M Hauck, Dawn A Brooks, Emily C Collins, Stephen Salloway, Mark A Mintun, John R Sims","doi":"10.1016/j.tjpad.2025.100266","DOIUrl":"10.1016/j.tjpad.2025.100266","url":null,"abstract":"<p><p>The TRAILBLAZER-ALZ 6 study (NCT05738486) evaluated the effect of different donanemab dosing regimens on amyloid-related imaging abnormalities with edema/sulcal effusions (ARIA-E). The modified titration arm met the primary outcome and significantly reduced ARIA-E frequency compared with the standard dosing while maintaining a similar pharmacodynamic effect on amyloid reduction at 24 weeks. Primary outcome and 52-week data were previously published. Completed study results at 76 weeks are reported here. ARIA-E frequencies were 15.6 % and 24.2 % in the modified titration and standard arms, respectively. ARIA-E radiographic severity was significantly lower (p = 0.015) with modified titration than with standard dosing. Additionally, symptomatic ARIA-E frequency was lower with modified titration versus standard dosing (2.8 % vs 4.8 %). The frequency of serious adverse events was comparable between the modified titration and standard dosing arms. A more gradual titration of donanemab dosing significantly reduced ARIA-E risk versus standard dosing. CLINICALTRIALS.GOV: NCT05738486.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100266"},"PeriodicalIF":7.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12413699/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144576227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adherence to an anti-inflammatory diet is associated with lower Alzheimer's disease mortality: A modifiable risk factor in a national cohort.","authors":"Ching-Chi Hsu, Shiow-Ing Wang, Sebastian Yu, Eric S Lin, James Cheng-Chung Wei","doi":"10.1016/j.tjpad.2025.100221","DOIUrl":"10.1016/j.tjpad.2025.100221","url":null,"abstract":"<p><strong>Background: </strong>Chronic neuroinflammation contributes to Alzheimer's disease (AD) pathogenesis, and diet is a modifiable factor influencing inflammation. The impact of an anti-inflammatory diet on AD-specific mortality remains unclear.</p><p><strong>Objectives: </strong>To examine the association between adherence to an anti-inflammatory diet (measured as the percentage of dietary energy from anti-inflammatory foods) and AD-specific mortality, as well as all-cause mortality, in a large national cohort, and to determine whether associations differ by sex or race/ethnicity.</p><p><strong>Methods: </strong>We analyzed 18,795 U.S. adults (≥18 years) from the 2007-2014 National Health and Nutrition Examination Survey. Anti-inflammatory diet adherence was defined as the percentage of total energy intake from anti-inflammatory foods, categorized as 0 %, <5 %, 5-9.99 %, or ≥10 %. Outcomes were AD-specific mortality and all-cause mortality ascertained via the National Death Index. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95 % confidence intervals (CIs) for mortality across intake categories, adjusting for demographic, lifestyle, and health factors. Analyses were stratified by sex, race/ethnicity, and age (≥45 years for AD mortality).</p><p><strong>Results: </strong>Participants with 0 % anti-inflammatory intake had a higher all-cause mortality risk (HR 3.82, 95 % CI 1.18-12.33) compared to those with ≥10 % intake. In the overall analysis, 0 % anti-inflammatory intake showed a trend of reduced AD-specific mortality although its did not reach statistical significance after full adjustment (HR 3.04, 95 % CI 0.74-12.46 vs. ≥10 % intake; p>0.05). Notably, the inverse association between anti-inflammatory diet and AD mortality emerged in subgroup analyses. Male participants and non-Hispanic White participants with 0 % intake had the highest AD mortality hazards (HR 12.83 and 3.77, respectively, vs. ≥10 % intake), indicating significant risk reductions with anti-inflammatory diet in these groups. In contrast, no significant associations were observed in female or non-White subgroups. Even a modest intake of anti-inflammatory foods (≥10 % of calories) was associated with lower AD mortality risk in the above subgroups and with lower all-cause mortality overall.</p><p><strong>Conclusion: </strong>Greater consumption of anti-inflammatory foods was associated with lower all-cause and a trend toward lower AD-specific mortality. The observed protective effects were confined to certain subpopulations (notably men and non-Hispanic Whites). Even a small portion of the diet (10 % of calories) being anti-inflammatory was linked to reduced mortality risk in these groups, suggesting that achievable dietary changes could have an impact. These findings support modifying dietary content is a practical, low-cost intervention that could mitigate neuroinflammation to reduce AD mortality risk.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100221"},"PeriodicalIF":7.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12413709/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144294875","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Household fuel use and motoric cognitive risk syndrome among older adults: Evidence from cohort study and life course analysis.","authors":"Guanghui Cui, Shaojie Li, Weiwei Li, Xuezhi Zhang","doi":"10.1016/j.tjpad.2025.100227","DOIUrl":"10.1016/j.tjpad.2025.100227","url":null,"abstract":"<p><strong>Background: </strong>Motoric cognitive risk syndrome (MCRS) is a predementia syndrome, and its prevention is valuable for reducing the incidence of dementia. However, few studies have focused on the association between indoor air pollution caused by household cooking fuel use and MCRS. This study aimed to investigate whether clean cooking fuel use is associated with reduced MCRS risk and whether the timing of clean fuel adoption across the life span is associated with MCRS prevalence.</p><p><strong>Methods: </strong>We used data from the China Health and Retirement Longitudinal Study. A prospective cohort analysis (n = 4251) examined baseline fuel use (2011) and incident MCRS over four years. A cross-sectional life course analysis (n = 6964) linked retrospective fuel use histories (2014 life history survey) to MCRS status in 2015. Modified Poisson regression was used to estimate relative risks (RRs) and 95 % confidence intervals (CIs), adjusting for covariates.</p><p><strong>Results: </strong>In the cohort study, clean fuel use at baseline was associated with a reduced risk of MCRS (RR = 0.76; 95 % CI: 0.61-0.96). Lower risks were also observed among participants who transitioned from solid to clean fuels and those who consistently used clean fuels. In the life course analysis, clean fuel adoption in early or middle adulthood was linked to lower MCRS prevalence.</p><p><strong>Conclusion: </strong>Clean fuel use for cooking and transitioning from solid to clean fuels decreases MCRS risk among older adults. Moreover, earlier adoption of clean cooking fuels is associated with a lower prevalence of MCRS in later life.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100227"},"PeriodicalIF":7.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12413735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144249692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The coupling of global brain activity and cerebrospinal fluid flow as a potential predictive marker of brain amyloid-β accumulation.","authors":"Yuya Tanaka, Koji Kamagata, Yuya Saito, Kaito Takabayashi, Rinako Iseki, Wataru Uchida, Christina Andica, Akifumi Hagiwara, Akihiko Wada, Toshiaki Akashi, Osamu Abe, Shigeki Aoki","doi":"10.1016/j.tjpad.2025.100228","DOIUrl":"10.1016/j.tjpad.2025.100228","url":null,"abstract":"<p><strong>Background: </strong>Impaired cerebrospinal fluid (CSF) clearance is thought to contribute to amyloid-β (Aβ) accumulation in Alzheimer's disease (AD). Global brain activity-CSF flow coupling (gBOLD-CSF coupling), measured through resting-state functional MRI, reflects CSF clearance capacity. A higher coupling value indicates weaker coupling. Its potential as a predictive marker for Aβ accumulation remains unclear.</p><p><strong>Objectives: </strong>This study aims to determine whether weaker gBOLD-CSF coupling precedes Aβ accumulation in cognitively normal, Aβ-negative individuals and to explore its predictive potential for amyloid conversion.</p><p><strong>Design: </strong>A longitudinal observational study using Alzheimer's Disease Neuroimaging Initiative (ADNI) data.</p><p><strong>Setting: </strong>Data from ADNI-participating sites.</p><p><strong>Participants: </strong>16 cognitively normal participants, initially Aβ-negative: seven fast-converters (transitioned to Aβ-positive within two years) and nine slow-converters (remained Aβ-negative for at least two years).</p><p><strong>Measurements: </strong>gBOLD-CSF coupling was calculated as the Pearson correlation coefficient between global Blood-Oxygen-Level-Dependent (BOLD) and CSF inflow signals. Group differences in gBOLD-CSF coupling were analyzed, along with partial correlation analyses between gBOLD-CSF coupling and annual changes in Aβ biomarkers and cognitive scores.</p><p><strong>Results: </strong>Fast-converters showed significantly higher gBOLD-CSF coupling values, indicating weaker coupling (Cohen's d = 1.76, p = 0.012). Coupling values positively correlated with annual changes in Aβ-PET SUVR (r = 0.594, p = 0.054) and negatively with MoCA scores (r = -0.654, p = 0.021).</p><p><strong>Conclusion: </strong>Weaker gBOLD-CSF coupling precedes brain Aβ accumulation, indicating its potential as a predictive marker for amyloid conversion. Future studies should refine clinical thresholds for early intervention strategies in AD prevention.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100228"},"PeriodicalIF":7.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12413707/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144294880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The differential effect of strength, cognitive and aerobic training combinations on cognitive performance and functional abilities in elderly with cognitive decline: The Fit4Alz project.","authors":"Ana Filipa Silva, Gilmara Assis, Rui Miguel Silva, Eugenia Murawska-Ciałowicz, Grzegorz Zurek, José Carvalho, Mafalda Sofia Roriz, José Alberto Azevedo, António Sampaio, Telmo Bento, Olivera Jovanovic, Marko Adamovic, Spartaco Grieco, Roberta Germini, Filipe Manuel Clemente","doi":"10.1016/j.tjpad.2025.100267","DOIUrl":"10.1016/j.tjpad.2025.100267","url":null,"abstract":"<p><strong>Background: </strong>Despite the global impact of neurodegenerative diseases and ongoing research efforts, pharmacological therapies have shown limited benefits. In contrast, physical exercise, with no side effects, has emerged as a non-pharmacological alternative that can enhance brain structure and function, promoting a healthier neurological phenotype.</p><p><strong>Objectives: </strong>This study aimed to explore the effects of aerobic and strength training methods, both with and without cognitive training, on mitigating or reversing cognitive decline in older adults.</p><p><strong>Design, setting, participants: </strong>In a randomized controlled trial, a total of 350 participants (average age 72.9 ± 6.0 years, 79 % female), with signs of decline (MoCA score below 26), were assigned to one of five groups: i) strength plus cognitive training (STCT, n = 92); ii) strength training (ST, n = 41); iii) aerobic training (AT, n = 97); iv) aerobic plus cognitive training (ATCT, n = 91); v) control (CG, n = 29).</p><p><strong>Intervention: </strong>For 12 weeks, all groups followed a 60 min training session three times a week, tailored to their specific group, with half of the sample adding 20 min of cognitive stimulation after the physical exercise.</p><p><strong>Measurements: </strong>Cognitive and physical assessments were conducted at the start and end of the intervention using the MoCA and the Senior Fitness test. A mixed ANCOVA analysis revealed significant interactions between time and group for all tests.</p><p><strong>Results: </strong>After the intervention, the CG showed significantly lower scores compared to all experimental groups. The CG also performed significantly worse than the ATCT group (p < 0.001). Additionally, the ATCT outperformed the STCT in the 6-min walk test (p < 0.05), while the STCT showed superior performance in the flexibility tests (sit and reach, back scratch) compared to the CG (p < 0.05).</p><p><strong>Conclusions: </strong>Results showed that 12-weeks of aerobic and strength training, with or without cognitive components, improved cognitive performance in older adults with cognitive decline, highlighting the importance of maintaining functional abilities for preserving skills, autonomy, independence, and quality of life in aging.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100267"},"PeriodicalIF":7.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12413704/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144609584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}