{"title":"Dietary patterns and blood-based biomarkers of Alzheimer's disease in cognitively intact older adults: Findings from a population-based study.","authors":"Anja Mrhar, Adrián Carballo-Casla, Giulia Grande, Martina Valletta, Claudia Fredolini, Laura Fratiglioni, Milica Gregorič Kramberger, Aleš Kuhar, Bengt Winblad, Amaia Calderón-Larrañaga, Davide Liborio Vetrano","doi":"10.1016/j.tjpad.2025.100124","DOIUrl":"10.1016/j.tjpad.2025.100124","url":null,"abstract":"<p><strong>Background: </strong>Diet can impact cognitive aging, but comprehensive data from human studies is lacking and the underlying biological mechanisms are still not fully understood.</p><p><strong>Objectives: </strong>To investigate the associations between two dietary patterns consistently linked to inflammation and brain health [the Mediterranean diet (MDS) and inflammatory potential of diet (EDII)] and five blood-based biomarkers of Alzheimer´s disease (AD) in a sample of dementia-free community-dwelling older adults.</p><p><strong>Design and setting: </strong>We used cross-sectional data from the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K).</p><p><strong>Participants: </strong>Participants who were institutionalized, had dementia or Parkinson's disease, or had missing data on diet and/or biomarkers were excluded. Our study sample consisted of 1907 adults ≥60 years old.</p><p><strong>Measurements: </strong>Adherence to the MDS and EDII was assessed using a validated food frequency questionnaire. T-tau, p-tau181, Aβ 42/40, NfL, and GFAP were measured in serum. Associations were estimated through quantile regression models at the 25th, 50th, and 75th percentiles of the biomarkers' levels, and were adjusted for potential confounders and stratified by sex, age, and APOE-e4 genotype.</p><p><strong>Results: </strong>In the whole sample, higher adherence to the MDS was associated with lower levels of p-tau181 at the 50th and 75th percentiles [β (95% CI) per 1-SD increment = -0.028 (-0.053, -0.002) and -0.036 (-0.072, -0.001), respectively], while higher adherence to the EDII was associated with higher levels of NfL at the 75th percentile [β (95% CI) per 1-SD increment =0.031 (0.008, 0.053)]. Associations with other biomarkers were only apparent at lower levels of their distribution. Subgroup analyses showed: 1) a stronger inverse association between the MDS and p-tau181 in APOE-e4 carriers than non-carriers, and 2) an inverse association of the MDS with GFAP only in participants ≥78 years.</p><p><strong>Conclusions: </strong>Diet seems to be associated with biomarkers of AD pathology in cognitively intact older adults. Some associations were more apparent in the presence of genetic predisposition for AD or advanced age.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100124"},"PeriodicalIF":4.3,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143634497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Brain health PRO/santé cerveau PRO: The development of a web-based program for dementia literacy and risk factor reduction.","authors":"Alex Bahar-Fuchs","doi":"10.1016/j.tjpad.2025.100206","DOIUrl":"10.1016/j.tjpad.2025.100206","url":null,"abstract":"","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100206"},"PeriodicalIF":4.3,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144111992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Not a slam dunk (or Free Lunch): The complex future of Alzheimer's combination therapy.","authors":"Cristina Sampaio","doi":"10.1016/j.tjpad.2025.100211","DOIUrl":"10.1016/j.tjpad.2025.100211","url":null,"abstract":"","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100211"},"PeriodicalIF":4.3,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144200050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Heidi J Welberry, Li-Jung Elizabeth Ku, Sophy Tf Shih, Louisa R Jorm, Maria Fiatarone Singh, Michael Valenzuela, Jeewani Anupama Ginige, Kaarin J Anstey, Perminder S Sachdev, John J McNeil, Nicola T Lautenschlager, Megan Heffernan, Tiffany Chau, Henry Brodaty
{"title":"The cost-effectiveness of an online intervention to prevent dementia: Results from the Maintain Your Brain (MYB) randomised controlled trial.","authors":"Heidi J Welberry, Li-Jung Elizabeth Ku, Sophy Tf Shih, Louisa R Jorm, Maria Fiatarone Singh, Michael Valenzuela, Jeewani Anupama Ginige, Kaarin J Anstey, Perminder S Sachdev, John J McNeil, Nicola T Lautenschlager, Megan Heffernan, Tiffany Chau, Henry Brodaty","doi":"10.1016/j.tjpad.2025.100151","DOIUrl":"10.1016/j.tjpad.2025.100151","url":null,"abstract":"<p><strong>Background: </strong>The Maintain Your Brain (MYB) randomised controlled trial (RCT) examined the effect of a multi-domain internet-based dementia prevention program against a control group (information only).</p><p><strong>Objectives: </strong>A cost-effective analysis (CEA) quantified the differences in costs (direct healthcare and program costs) and effectiveness outcomes between the intervention and control groups from a healthcare sector perspective.</p><p><strong>Design: </strong>An economic evaluation was conducted alongside the MYB RCT over three years.</p><p><strong>Setting: </strong>Australians aged 55-77 years with at least 2 identified remediable risk factors for cognitive decline/dementia recruited from communities in New South Wales.</p><p><strong>Participants: </strong>There were 3,025 participants in the intervention group and 3,033 in the control group with available linked healthcare data via the Sax Institute's 45 and Up Study out of the 6104 enrolled in the trial (99.2% of total cohort).</p><p><strong>Intervention: </strong>The MYB trial comprised a personalised schedule of online coaching in physical activity, nutrition, cognitive activity, and depression or anxiety management.</p><p><strong>Measurements: </strong>The two effectiveness outcomes were global cognition composite (GCC) scores and the Australian National University-Alzheimer's Disease Risk Index -short form (ANU-ADRI-SF) questionnaire scores. Costs included MYB program costs and the direct healthcare costs incurred by the MYB participants. All costs were reported in Australian dollars (AUD$) during the trial period. The time horizon of this analysis was 3 years after randomisation (2018-2021). Incremental cost-effectiveness ratio (ICERs) between the intervention and the control groups were calculated by comparing the average difference in costs to a mean difference in z score for GCC and ANU-ADRI-SF score using the bootstrapped means and 95% Confidence Intervals.</p><p><strong>Results: </strong>The total unadjusted program and healthcare costs over three years were similar between groups (AUD$16,521 per person in the control group and AUD$16,473 in the intervention group). After adjusting for baseline characteristics, the average difference between groups in total cost per person at three years was not statistically different: AUD$467 favouring the control group (95%CI: -$552 - $1585). This was compared to a significant mean difference (improvement) in GCC z score at three years of 0.18 (95%CI: 0.13, 0.23) and -0.57 (95%CI: -0.95, -0.24) point difference in ANU-ADRI-SF for the intervention versus control. The base case ICERs were AUD$2,568 per 1 standard deviation in z score and $823 per reduction of 1 ANU-ADRI-SF point. With 1000 bootstrapped replications, the scatterplots of ICER ellipses suggest that the MYB intervention was more effective than the control group and with no significant difference in overall healthcare costs.</p><p><strong>Conclusion:","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100151"},"PeriodicalIF":4.3,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143796576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Caroline Robert, Lieng-Hsi Ling, Eugene S J Tan, Narayanaswamy Venketasubramanian, Shir Lynn Lim, Lingli Gong, Josephine Lunaria Berboso, Arthur Mark Richards, Christopher Chen, Saima Hilal
{"title":"Longitudinal associations of carotid artery stiffness with progression of cerebrovascular disease, incident dementia and cognitive decline in older adults.","authors":"Caroline Robert, Lieng-Hsi Ling, Eugene S J Tan, Narayanaswamy Venketasubramanian, Shir Lynn Lim, Lingli Gong, Josephine Lunaria Berboso, Arthur Mark Richards, Christopher Chen, Saima Hilal","doi":"10.1016/j.tjpad.2025.100127","DOIUrl":"10.1016/j.tjpad.2025.100127","url":null,"abstract":"<p><strong>Background: </strong>Carotid artery stiffness is associated with cerebrovascular disease (CeVD) and cognitive impairment, but evidence for its longitudinal effects on progression of CeVD and cognitive decline are limited.</p><p><strong>Objectives: </strong>To evaluate the longitudinal associations of carotid artery stiffness with CeVD progression, incident dementia, and cognitive decline.</p><p><strong>Design: </strong>Longitudinal analyses from a memory-clinic cohort with a follow-up of 2 years.</p><p><strong>Setting: </strong>A memory-clinic study.</p><p><strong>Participants: </strong>194 participants (mean age=80, 63 % female) with or without cognitive impairments provided consent to take part in the study.</p><p><strong>Measurements: </strong>Participants underwent carotid ultrasonography, brain MRI, and neuropsychological assessments were at baseline and follow-up. Carotid stiffness measures included ß-index, elastic modulus (Ep), and pulse wave velocity-ß (PWV-ß). CeVD markers included white matter hyperintensities (WMH), lacunes, cerebral microbleeds (CMBs) and cortical infarcts. Cognition was assessed with a neuropsychological battery.</p><p><strong>Results: </strong>After 2 years, incident CeVD cases included lacunes (15.7 %), CMBs (23.8 %), and cortical infarcts (7.6 %). ß-index (ß=0.78, p < 0.001), Ep (ß=0.94, p < 0.001), and PWV-ß (ß=0.15, p = 0.003) were independently associated with WMH progression. Ep (ß=-0.15, p = 0.007) and PWV-ß (ß=-3.68, p = 0.007) were independently associated with visuomotor speed decline. No association was found with incident lacunes, CMBs or dementia.</p><p><strong>Conclusion: </strong>Carotid stiffness progression is associated with WMH progression and visuomotor speed decline.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100127"},"PeriodicalIF":4.3,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143597728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Haonan Li, Meng Cheng, Nannan Zhang, Siqi Wang, Caihua Ye, Haodong Li, Shengnan Wang, Zirui Wang, Xuan Yang, Zhixuan Liu, Xingyu Zhang, Jiayuan Xu, Qiang Xu, Junping Wang
{"title":"The role of serum vitamins in mediating the effect of neurodegenerative diseases on subcortical brain volume.","authors":"Haonan Li, Meng Cheng, Nannan Zhang, Siqi Wang, Caihua Ye, Haodong Li, Shengnan Wang, Zirui Wang, Xuan Yang, Zhixuan Liu, Xingyu Zhang, Jiayuan Xu, Qiang Xu, Junping Wang","doi":"10.1016/j.tjpad.2025.100155","DOIUrl":"10.1016/j.tjpad.2025.100155","url":null,"abstract":"<p><strong>Background: </strong>Neurodegenerative diseases (NDs) lead to a progressive loss of neuronal cells and link to atrophy of subcortical brain structures, but the causal intermediates are not known. To test whether major NDs (Alzheimer's disease (AD), Parkinson's disease, multiple sclerosis, and amyotrophic lateral sclerosis) causally affects subcortical atrophy, and whether serum vitamin level play a mediating role in this process.</p><p><strong>Methods: </strong>Using large-scale genome-wide association study (GWAS) summary data, we performed two-sample Mendelian randomization (MR) to assess the causal effect of NDs on the volume of seven subcortical structures, and then adopted two-step multivariable MR approach to quantify the proportion of the effect of NDs on the volume of subcortical regions mediated by serum vitamin level. Finally, we utilized animal experiments to validate results and explored the potential molecular mechanisms.</p><p><strong>Results: </strong>Genetically predicted AD was associated with atrophy of the nucleus accumbens (NAc) (β = -0.09; p = 5.13 × 10<sup>-5</sup>), amygdala (β = -0.07; p = 8.44 × 10<sup>-4</sup>), and hippocampus (β = -0.07; p = 0.001), as well as with low serum vitamin D level (β = -0.02; p = 6.84 × 10<sup>-6</sup>). Specifically, decreased serum vitamin D level mediated 3.99 % (95 % CI: -0.006 to -5.82 × 10<sup>-5</sup>) and 3.97 % (95 % CI: -0.007 to -2.94 × 10<sup>-4</sup>) of the total effect of AD on hippocampal and NAc atrophy, respectively. Animal experiments further confirmed significant delays in hippocampal and NAc atrophy, a significant reduction of β-amyloid deposits and an increase of vitamin D receptor expression in hippocampus in AD mice with high-dose vitamin D diet.</p><p><strong>Conclusions: </strong>These findings provide important insights into the effect sizes of vitamin D-mediated roles in AD and atrophy of subcortical structures. Interventions to increase serum vitamin D levels at a population level might attenuate damage to hippocampus in patients with AD.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100155"},"PeriodicalIF":4.3,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143781191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Suhang Song, Meng Hsuan Sung, Diana Diaz, Zhuofan Lin, Allan D Tate, Zhuo Chen, Janani Rajbhandari-Thapa, Grace Bagwell Adams, M Mahmud Khan, Ye Shen, Lisa M Renzi-Hammond, Yinzi Jin
{"title":"Long-term cumulative physical activity associated with less cognitive decline: Evidence from a 16-year cohort study.","authors":"Suhang Song, Meng Hsuan Sung, Diana Diaz, Zhuofan Lin, Allan D Tate, Zhuo Chen, Janani Rajbhandari-Thapa, Grace Bagwell Adams, M Mahmud Khan, Ye Shen, Lisa M Renzi-Hammond, Yinzi Jin","doi":"10.1016/j.tjpad.2025.100194","DOIUrl":"10.1016/j.tjpad.2025.100194","url":null,"abstract":"<p><strong>Introduction: </strong>Physical activity (PA) has been reported to delay cognitive decline. However, the role of long-term, cumulative PA (cPA) in cognitive decline remains unclear.</p><p><strong>Methods: </strong>This longitudinal study obtained data from Health and Retirement Study, 2004-2020. Global cognition was operationalized as the sum of memory and executive function scores on a battery of cognitive tests. cPA was operationalized as the area under the curve of the metabolic equivalent of tasks (MET) adjusted PA. Generalized linear mixed models were fitted to examine the associations between cPA and cognitive change.</p><p><strong>Results: </strong>This study included 13,450 cognitively healthy participants, with a mean follow-up duration of 11.06 (SD=4.91) years. Higher cPA was associated with delayed declines in global cognition (p<.001), memory (p<.001) and executive function (p<.001), and such protective benefits grew over the 16-year study period. Longer PA engagement was associated with progressively delayed cognitive decline.</p><p><strong>Conclusion: </strong>PA engagement over long timeframes may better maintain cognitive performance.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100194"},"PeriodicalIF":4.3,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144015234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Response to \"Multi-omics analysis of druggable genes to facilitate Alzheimer's disease therapy: A multi-cohort machine learning study\".","authors":"Jichang Hu","doi":"10.1016/j.tjpad.2025.100250","DOIUrl":"10.1016/j.tjpad.2025.100250","url":null,"abstract":"","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100250"},"PeriodicalIF":4.3,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144529618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Association between the use of information and communication technology and cognitive decline stratified by social isolation: The Otassha study.","authors":"Keigo Imamura, Hisashi Kawai, Manami Ejiri, Hiroyuki Sasai, Kazushige Ihara, Harumi Nakada, Atsushi Araki, Hirohiko Hirano, Yoshinori Fujiwara, Takao Suzuki, Shuichi Obuchi","doi":"10.1016/j.tjpad.2025.100138","DOIUrl":"10.1016/j.tjpad.2025.100138","url":null,"abstract":"<p><strong>Background: </strong>Prevention of dementia is crucial for reducing its social burden. Social isolation is a known risk factor for dementia. The use of information and communication technology is associated with reduced cognitive decline. However, longitudinal associations of the use of information and communication technology with cognitive function remain unknown, especially for older adults who are socially isolated and at a high risk of cognitive decline.</p><p><strong>Objectives: </strong>To investigate the association between the use of information and communication technology and changes in cognitive function among older adults with and without social isolation.</p><p><strong>Design: </strong>Longitudinal observational study SETTING: Data was obtained for two cohorts of community-dwelling older adults aged 65 years with no cognitive impairment (Mini-Mental State Examination score ≥24) at baseline.</p><p><strong>Participants: </strong>Participants were defined as those who completed baseline assessments of the use of information and communication technology, social isolation, and cognitive function and underwent at least one follow-up assessment of cognitive function in a follow-up survey conducted annually through 2023.</p><p><strong>Measurements: </strong>The use of information and communication technology was measured using the technology usage sub-items of the Japan Science and Technology Agency Index of Competence. Cognitive function and social isolation were assessed using the Mini-Mental State Examination and the six-item Lubben Social Network Scale, respectively. Data from the two cohorts were combined to examine the association between the use of information and communication technology and changes in cognitive function, as well as the association between the use of information and communication technology and the incidence of cognitive decline (Mini-Mental State Examination <24), using mixed effects models and Cox proportional hazards models, respectively. These analyses were conducted separately based on social isolation.</p><p><strong>Results: </strong>A total of 1,322 participants (mean age: 72.3 years, 39 % male) were included in the final analysis. The median follow-up period was 3.9 years. Individuals who used information and communication technology experienced a slower rate of cognitive decline than non-users (-0.09, 95 % confidence interval: -0.11 to -0.07 vs. -0.18, 95 % confidence interval: -0.21 to -0.15). In addition, information and communication technology use was associated with a significantly lower risk of cognitive decline (hazard ratio: 0.73, 95 % confidence interval: 0.70-0.76). This association remained consistent among older adults with social isolation (hazard ratio: 0.91, 95 % confidence interval: 0.85-0.97).</p><p><strong>Conclusions: </strong>The use of information and communication technology was associated with a reduced risk of cognitive decline, even among socially isolated older adults. C","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100138"},"PeriodicalIF":4.3,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143721415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}