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

{"title":"Challenges and opportunities for novel combination therapies in Alzheimer's disease: a report from the EU/US CTAD Task Force.","authors":"D Angioni, L Middleton, R Bateman, P Aisen, A Boxer, S Sha, J Zhou, I Gerlach, R Raman, H Fillit, S Salloway, R Sperling, B Vellas, J Cummings","doi":"10.1016/j.tjpad.2025.100163","DOIUrl":"https://doi.org/10.1016/j.tjpad.2025.100163","url":null,"abstract":"<p><p>Following the recent approvals of anti-amyloid immunotherapies as \"first-in-kind\" disease-modifying agents for Alzheimer's disease (AD), there is an emerging emphasis in combination therapies, given the complex and multifactorial etiopathogenesis and pathophysiology of the disease. The EU/US CTAD Task Force met in Madrid in October 2024, to discuss biological rationale and methodological issues and outline potential directions for future research in combination therapies. The Task Force agreed on the necessity and urgency of advancing combination therapies for AD treatment. As of January 1, 2024, in the drug development pipeline, there were 21 combination trials (13 % of all trials). The combination of anti-amyloid and anti-tau therapies could become a central focus of the field. Combinations involving anti-inflammatory and immune mechanisms with anti-amyloid or other therapies also have promise. To facilitate the development and implementation of combination therapies, collaborations between sponsors and public-private partnerships are essential. Optimizing the likelihood of success primarily requires leveraging the use of biomarkers and a clearer understanding of the biological mechanisms underpinning AD and their interactions, especially those involving amyloid, tau, and inflammation, that lead to cognitive decline and progression.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100163"},"PeriodicalIF":4.3,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144047374","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":"Using machine learning and electronic health record (EHR) data for the early prediction of Alzheimer's Disease and Related Dementias.","authors":"Sonia Akter, Zhandi Liu, Eduardo J Simoes, Praveen Rao","doi":"10.1016/j.tjpad.2025.100169","DOIUrl":"https://doi.org/10.1016/j.tjpad.2025.100169","url":null,"abstract":"<p><strong>Background: </strong>Over 6 million patients in the United States are affected by Alzheimer's Disease and Related Dementias (ADRD). Early detection of ADRD can significantly improve patient outcomes through timely treatment.</p><p><strong>Objective: </strong>To develop and validate machine learning (ML) models for early ADRD diagnosis and prediction using de-identified EHR data from the University of Missouri (MU) Healthcare.</p><p><strong>Design: </strong>Retrospective case-control study.</p><p><strong>Setting: </strong>The study used de-identified EHR data provided by the MU NextGen Biomedical Informatics, modeled with the PCORnet Common Data Model (CDM).</p><p><strong>Participants: </strong>An initial cohort of 380,269 patients aged 40 or older with at least two healthcare encounters was narrowed to a final dataset of 4,012 ADRD cases and 119,723 controls.</p><p><strong>Methods: </strong>Six ML classifier models: Gradient-Boosted Trees (GBT), Light Gradient-Boosting Machine (LightGBM), Random Forest (RF), eXtreme Gradient-Boosting (XGBoost), Logistic Regression (LR), and Adaptive Boosting (AdaBoost) were evaluated using Area Under the Receiver Operating Characteristic Curve (AUC-ROC), accuracy, sensitivity, specificity, and F1 score. SHAP (SHapley Additive exPlanations) analysis was applied to interpret predictions.</p><p><strong>Results: </strong>The GBT model achieved the best AUC-ROC scores of 0.809-0.833 across 1- to 5-year prediction windows. SHAP analysis identified depressive disorder, age groups 80-90 yrs and 70-80 yrs, heart disease, anxiety, and the novel risk factors of sleep apnea, and headache.</p><p><strong>Conclusion: </strong>This study underscores the potential of ML models for leveraging EHR data to enable early ADRD prediction, supporting timely interventions, and improving patient outcomes. By identifying both established and novel risk factors, these findings offer new opportunities for personalized screening and management strategies, advancing both clinical and informatics science.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100169"},"PeriodicalIF":4.3,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144035733","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":"Multimorbidity and risk of dementia: A systematic review and meta-analysis of longitudinal cohort studies.","authors":"Yaguan Zhou, Yating You, Yuting Zhang, Yue Zhang, Changzheng Yuan, Xiaolin Xu","doi":"10.1016/j.tjpad.2025.100164","DOIUrl":"https://doi.org/10.1016/j.tjpad.2025.100164","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Chronic diseases (e.g., hypertension, diabetes, and heart diseases) have been proposed as marked predictors of incident dementia. However, synthesised evidence on the effect of multimorbidity on dementia is still lacking. We aim to summarise the association between multimorbidity and risk of dementia in longitudinal cohorts.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;In this systematic review and meta-analysis, we conducted a systematic search in PubMed, Web of Science and Embase from inception to Dec 14, 2024, to identify longitudinal cohort studies reporting the association between multimorbidity or multimorbidity patterns and risk of dementia. Information of included studies were extracted by three reviewers (YaZ, YY and YuZ), and the quality assessment was conducted using the Newcastle-Ottawa Scale. The inverse-variance weighted random effects meta-analysis was performed to obtain the pooled hazard ratios (HRs) and 95 % confidence intervals (CIs) for dementia associated with multimorbidity and cardiometabolic multimorbidity (CMM). Cochran's Q test and the I&lt;sup&gt;2&lt;/sup&gt; statistic were used to indicate heterogeneity among the studies. Meta-regression analysis, subgroup analysis and sensitivity analysis were conducted to determine any valid sources of heterogeneity. This study was registered with PROSPERO (CRD42023403684).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;We included 17 longitudinal cohort studies (2262,885 middle-aged and older participants) in the systematic review, of which seven were included in meta-analysis. All studies presented moderate to high methodological quality. Meta-analysis showed a positive association between multimorbidity and incident dementia (HR=1.53, 95 % CI=1.12 to 2.09), with substantial heterogeneity (I&lt;sup&gt;2&lt;/sup&gt;=95.2 %). Studies using health records to measure dementia tend to find a stronger positive relationship between multimorbidity and risk of dementia than those using self-report (HR&lt;sub&gt;health records&lt;/sub&gt;=1.94, 95 % CI=1.35 to 2.78, I&lt;sup&gt;2&lt;/sup&gt;=94 %; HR&lt;sub&gt;self-report&lt;/sub&gt;=1.17, 95 % CI=1.07 to 1.28, I&lt;sup&gt;2&lt;/sup&gt;=0 %). The impacts of CMM were also observed, and the HRs for dementia ranged from 2.49 (combination of heart diseases and stroke: 95 % CI=1.64 to 3.78) to 3.77 (combination of diabetes, heart diseases and stroke: 95 % CI=2.02 to 7.02). The heterogeneity was moderate, with I&lt;sup&gt;2&lt;/sup&gt; ranging from 46.9 % (p for heterogeneity=0.152) to 84.1 % (p for heterogeneity=0.002). The impacts of number of diseases, multimorbidity clusters, and multimorbidity trajectory on risk of dementia were narratively summarised due to lacking comparable studies. Limited evidence (only one study) precluded quantitative synthesis for the association of physical and psychological multimorbidity with dementia.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;Multimorbidity and CMM pattern were significantly associated with risk of dementia, while the effect of physical and psychological multimorbidity remain incon","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100164"},"PeriodicalIF":4.3,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144013640","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":"Disparities in out-of-pocket costs for disease-modifying therapy under Japan's universal health insurance system.","authors":"Kenichiro Sato, Ryoko Ihara, Yoshiki Niimi, Saki Nakashima, Atsushi Iwata, Takeshi Iwatsubo","doi":"10.1016/j.tjpad.2025.100170","DOIUrl":"https://doi.org/10.1016/j.tjpad.2025.100170","url":null,"abstract":"","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100170"},"PeriodicalIF":4.3,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998823","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":"Herpes zoster as risk factor for dementia: a matched cohort study over 20 years in a 10-million population in Italy.","authors":"Lorenzo Blandi, Paola Bertuccio, Carlo Signorelli, Helmut Brand, Timo Clemens, Cristina Renzi, Anna Odone","doi":"10.1016/j.tjpad.2025.100167","DOIUrl":"https://doi.org/10.1016/j.tjpad.2025.100167","url":null,"abstract":"<p><strong>Background: </strong>Herpes Zoster is caused by the reactivation of the Varicella-Zoster Virus. Zoster may influence the occurrence of dementia, but contradictory results about this association emerged from recent studies. These findings did not consider the severity of Zoster and observed individuals for limited follow-up time. Our study used a region-wide Italian registry to investigate the association between severe Zoster infection and dementia occurrence over a 23-year period.</p><p><strong>Methods: </strong>We included people aged ≥ 50 and hospitalised with Zoster, and two comparison cohorts from both the general population and the hospitalised population without Zoster. By random sampling, the matching 1:5 was based on sex, birth year, and entry date in the cohort. Dementia and Zoster were identified through validated algorithms. A Fine-Gray sub-distribution hazard model was used, accounting for competing risk of death.</p><p><strong>Results: </strong>We identified 132,968 individuals, of whom 12,088 with severe Zoster, 60,440 matched controls among the general population, and 60,440 matched controls among the hospitalised population. In severe cases of Herpes Zoster, the overall adjusted sub-distributed hazard ratio of dementia was 1.13 (95 % CI 1.07-1.19) compared to the general population, and 1.08 (95 % CI 1.03-1.14) compared to hospitalised population. Hazard ratios were still significant in different strata group, including by sex, age group (including in 50-65 younger adults) and at different follow-up period.</p><p><strong>Conclusions: </strong>Our population-based study found an increased risk of developing dementia among severe Zoster cases. Those results support the importance of improving Zoster prevention and extending the vaccination recommendations to younger age groups.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100167"},"PeriodicalIF":4.3,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144039539","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":"Associations between the EAT-Lancet planetary health diet and incident dementia.","authors":"Jessica Samuelsson, Isabelle Glans, Anna Stubbendorff, Ulrika Ericson, Sebastian Palmqvist, Oskar Hansson, Emily Sonestedt","doi":"10.1016/j.tjpad.2025.100166","DOIUrl":"https://doi.org/10.1016/j.tjpad.2025.100166","url":null,"abstract":"<p><strong>Background: </strong>The impact of the environmentally sustainable EAT-Lancet diet on dementia risk remains poorly understood. The aim was to investigate associations between the EAT-Lancet diet and incident dementia.</p><p><strong>Methods: </strong>Associations of the EAT-Lancet diet with all-cause dementia, Alzheimer's disease (AD), and vascular dementia (VaD) were investigated among 25,898 participants from the Malmö Diet and Cancer study, Sweden. Participants aged 45-73 years were recruited for the baseline examination between 1991 and 1996, and the mean follow-up time was 18 years. To assess robustness of estimations, we used seven previously constructed EAT-Lancet diet scores. Multi-adjusted Cox proportional hazard analyses were performed, with results presented per 10 % in increment scores. Additionally, we explored the potentially modifying effect of APOE ε4 status in this context.</p><p><strong>Results: </strong>With one of the scores, higher adherence to the EAT-Lancet diet was associated with a reduced risk of AD and all-cause dementia. Moreover, the results suggest an interplay between the EAT-Lancet diet and APOE ε4 status. A risk-reducing effect was observed among APOE ε4 non-carriers with three of the scores in relation to AD, and with five of the scores in relation to all-cause dementia. No associations were observed among APOE ε4 carriers, or in relation to VaD.</p><p><strong>Conclusion: </strong>The results indicate a risk reducing effect of adhering to the EAT-Lancet diet among APOE ε4 non-carriers, and no negative effects on dementia risk were detected. Future studies should consider the potentially modifying effect of APOE ε4 status, and the implications of methodological differences in measuring adherence to the EAT-Lancet diet.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100166"},"PeriodicalIF":4.3,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144019404","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":"Baseline habitual dietary nitrate intake and Alzheimer's Disease related neuroimaging biomarkers in the Australian Imaging, Biomarkers and Lifestyle study of ageing.","authors":"Anjana Rajendra, Nicola P Bondonno, Kevin Murray, Liezhou Zhong, Stephanie R Rainey-Smith, Samantha L Gardener, Lauren C Blekkenhorst, Vincent Doré, Victor L Villemagne, Simon M Laws, Belinda M Brown, Kevin Taddei, Colin L Masters, Christopher C Rowe, Ralph N Martins, Jonathan M Hodgson, Catherine P Bondonno","doi":"10.1016/j.tjpad.2025.100161","DOIUrl":"https://doi.org/10.1016/j.tjpad.2025.100161","url":null,"abstract":"<p><strong>Background: </strong>Dietary nitrate, as a nitric oxide (NO) precursor, may support brain health and protect against dementia.</p><p><strong>Objective: </strong>Our primary aim was to investigate whether dietary nitrate is associated with neuroimaging markers of brain health linked with Alzheimer's disease (AD).</p><p><strong>Participants: </strong>Study participants were cognitively unimpaired individuals from the Australian Imaging, Biomarkers and Lifestyle Study of Ageing (AIBL) who had β-amyloid positron emission tomography (PET) scans (n = 554) and magnetic resonance imaging (MRI) scans (n = 335) and had completed a Food Frequency Questionnaire at baseline.</p><p><strong>Methods: </strong>Source-specific nitrate intakes were estimated using comprehensive nitrate food composition databases. Rates of cerebral β-amyloid (Aβ) deposition, measured using PET, and rates of brain atrophy, measured using MRI, were assessed between baseline and 126-months follow-up, at intervals of 18 months. Multivariable-adjusted linear mixed effect models were used to examine associations between baseline source-specific nitrate intake and rates of (i) cerebral Aβ deposition and (ii) brain atrophy, over the 126 months of follow-up. Analyses were carried out following stratification of the sample by established dementia Alzheimer's disease (AD) risk factors including sex and presence or absence of the apolipoprotein E (APOE) ε4 allele.</p><p><strong>Results: </strong>In women carriers of the APOE ε4 allele, higher plant sourced nitrate intake (median intake 121 mg/day), was associated with a slower rate of cerebral Aβ deposition [β: 4.47 versus 8.99 Centiloid (CL) /18 months, p < 0.05] and right hippocampal atrophy [-0.01 versus -0.03 mm3 /18 months, p < 0.01], after multivariable adjustments. Moderate intake showed protective associations in men carriers and in both men and women non-carriers of APOE ε4.</p><p><strong>Conclusions: </strong>Associations were observed between plant-derived nitrate intake and cerebral Aβ deposition, particularly in high-risk populations (women and APOE ε4 carriers). Associations were also observed for brain volume atrophy, however these exhibited subgroup variability without clear patterns relative to sex and APOE ε4 allele carriage. These findings suggest a potential link between plant-sourced nitrate and AD related neuroimaging markers of brain health improved brain health, but further validation in larger studies is required.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100161"},"PeriodicalIF":4.3,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144034963","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":"Poor glymphatic function is associated with mild cognitive impairment and its progression to Alzheimer's disease: A DTI-ALPS study.","authors":"Cuiping Bao, Hongbin Luo, Jiao Wang, Xuehuan Liu, Yiming Li, Jun Yang, Chong Chen, Rongrong Yang, Weili Ba, Xinying Lian, Michelle Dunk, Jun Liu, Weili Xu","doi":"10.1016/j.tjpad.2025.100156","DOIUrl":"https://doi.org/10.1016/j.tjpad.2025.100156","url":null,"abstract":"<p><strong>Background: </strong>We aimed to explore the association between ALPS index and both risks of MCI from cognitively normal (CN) and incident AD progressed from MCI, as well as potential mediating factors.</p><p><strong>Methods: </strong>This study included 519 adults including 253 (48.75 %) CN and 266 (51.25 %) MCI participants from Alzheimer's Disease Neuroimaging Initiative. Glymphatic function (assessed by along the perivascular space [ALPS] index) was measured by diffusion tensor image at baseline. Neurobiomarkers (Aβ and tau from CSF, plasma and PET) and cognitive functions were served as mediators. Data were analyzed using Cox and Laplace regression and mediation analysis.</p><p><strong>Results: </strong>During follow-up (median 3.6 years, interquartile range [IQR]: 2.0-4.9 years), 30 (11.86 %) participants developed MCI in the CN cohort and 73 (27.4 %) participants progressed to AD in the MCI cohort. The hazard ratios (95 % confidence intervals [CIs]) of the higher ALPS index was 0.605 (0.386-0.948) for MCI and 0.501 (0.356-0.706) for AD. In addition, participants with high ALPS index had 3.837 and 3.466 years prolonged onset of MCI and AD, separately. Aβ in choroid plexus (17.1 %), tau in cortex [Inferiortemporal (21.1 %), Middletemporal (AV1451:17.0 %, FTP:15.5 %), Superiortemporal(7.7 %), Meta_temporal (AV1451:17.5 %, FTP:16.6 %)], and executive function (14.1 %) mediated the association between ALPS and MCI-AD progression.</p><p><strong>Conclusion: </strong>High ALPS index decreases MCI risk and delays MCI progression to AD by approximately 3.5 years. Aβ in choroid plexus, tau in cortex, and executive function may partially mediate the MCI-AD progression in relation to ALPS index.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100156"},"PeriodicalIF":4.3,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144049399","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":"Chronotype as a potential risk factor for cognitive decline: The mediating role of sleep quality and health behaviours in a 10-year follow-up study.","authors":"A N Wenzler, A C Liefbroer, R C Oude Voshaar, N Smidt","doi":"10.1016/j.tjpad.2025.100168","DOIUrl":"https://doi.org/10.1016/j.tjpad.2025.100168","url":null,"abstract":"<p><strong>Background: </strong>- With rising life expectancies and ageing populations worldwide, preserving cognitive health is an urgent global priority. Chronotype could be a potential risk factor for cognitive decline, potentially through mediators sleep quality, alcohol intake, physical activity, and smoking.</p><p><strong>Methods: </strong>- This study used data from participants aged 40 years and older from the Lifelines cohort study (n = 23,798). Chronotype, assessed with the Munich ChronoType Questionnaire, was included as a continuous score of mid-point sleep corrected for sleep debt on workdays. Multiple linear regression examined the association between chronotype and cognitive decline, including moderation by age, educational attainment, and sex. The KHB-method was applied to test mediation by sleep quality, alcohol intake, physical activity, and smoking.</p><p><strong>Outcomes: </strong>- Cognition was assessed with the Ruff Figural Fluency Test (RFFT), measuring non-verbal fluency and executive functioning. Cognitive decline was calculated by subtracting the RFFT sum score at baseline from the 10-year follow-up score.</p><p><strong>Results: </strong>- Chronotype was associated with cognitive decline. Educational attainment, but not age or sex, moderated the relationship. No significant associations were observed in the low- (0.07, 95 % CI: -0.44, 0.57) or middle- (-0.41, 95 % CI: -0.88, 0.06) educational groups. In the high-educational group each one-hour increase in chronotype corresponded to a 0.80-point decline in cognition per decade (95 % CI: -1.34, -0.26). In this group, sleep quality and current smoking mediated 13.52 % and 18.64 % of the association, respectively.</p><p><strong>Interpretation: </strong>- Chronotype was associated with greater decline in non-verbal fluency and executive functioning among higher educated participants, highlighting the importance of targeted prevention strategies.</p><p><strong>Funding: </strong>- This work is part of the BIRD-NL consortium funded by the Dutch Medical Research Council, ZonMw (Dementia research program) project number:10,510,032,120,005.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100168"},"PeriodicalIF":4.3,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143982909","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":"Lifestyle and cognition: Separating the effects of average lifestyle and lifestyle changes based on the LIBRA score.","authors":"Kej Wesenhagen, K Deckers, Hsj Picavet, M L Rietman, Aal Kok, S Köhler, M A Ikram, F J Wolters, M Huisman, Wmm Verschuren","doi":"10.1016/j.tjpad.2025.100159","DOIUrl":"https://doi.org/10.1016/j.tjpad.2025.100159","url":null,"abstract":"<p><strong>Background: </strong>The LIfestyle for BRAin Health (LIBRA) score, consisting of twelve factors, highlights individuals' potential for dementia risk reduction through lifestyle. The LIBRA score includes modifiable protective factors such as low to moderate alcohol consumption, and risk factors such as hypertension.</p><p><strong>Objective: </strong>We studied whether LIBRA scores are longitudinally associated with cognition, and to what extent this is due to between-person differences or within-person changes in LIBRA scores.</p><p><strong>Methods: </strong>Individuals were included from four Dutch community-based cohorts: Doetinchem Cohort Study (DCS; n = 4770), Maastricht Aging Study (MAAS; n = 1295), Longitudinal Aging Study Amsterdam (LASA; n = 2391) and the Rotterdam Study (RS; n = 5205). The number of available LIBRA components (range 7-11) and timepoints (range 3-9) differed per cohort. Outcomes were standardized processing speed (LDST), memory (15-word delayed recall of the verbal learning test (VLT)) and verbal fluency. Hybrid mixed models were fit for the association of 1) mean LIBRA score and 2) change in LIBRA between subsequent timepoints. Models were adjusted for age, sex, education and learning effects. Interactions of the mean LIBRA score with age, and change in LIBRA score with age were tested in two separate models.</p><p><strong>Results: </strong>Higher (i.e., unhealthier) mean LIBRA scores were associated with worse cognitive speed (lower LDST z-score per 1-point higher LIBRA, range between cohorts: 0.039 - 0.0587), memory (VLT, 0.026 - 0.035), and fluency (0.020 - 0.033). Associations of mean LIBRA scores with cognitive function were stronger with older age (LDST: significant age-interaction, 2 out of 4 cohorts; VLT and fluency: 1 out of 4 cohorts). Relative to 65-year-old individuals with a mean LIBRA score at the 50th percentile, individuals at the 90th percentile of the LIBRA score showed an estimated 1.9-3.2 years more advanced cognitive ageing for LDST, 1.9 - 5.3 years for VLT and 1.4 - 1.7 years for fluency. Within-person change in LIBRA showed no consistent associations with cognitive decline.</p><p><strong>Conclusions: </strong>An individual's mean LIBRA score, but not their change in LIBRA score over time, was longitudinally associated with cognitive functioning. In the general population, the investigated version of the LIBRA score is possibly not suitable to capture how cognition (as a proxy for dementia risk) changes with improvements in lifestyle.</p>","PeriodicalId":22711,"journal":{"name":"The Journal of Prevention of Alzheimer's Disease","volume":" ","pages":"100159"},"PeriodicalIF":4.3,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144039312","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}