GeroScience最新文献

{"title":"High-resolution glutamate-weighted mapping of in vivo mouse brain across age with chemical exchange saturation transfer MRI.","authors":"R Gaudin, T Delebarre, M Glatigny, E Selingue, C Debacker, L Ciobanu, D Boido","doi":"10.1007/s11357-026-02290-z","DOIUrl":"https://doi.org/10.1007/s11357-026-02290-z","url":null,"abstract":"<p><p>Aging in the mammalian brain involves significant structural, functional, and metabolic changes, including a decrease in glutamate concentration. Glutamate-weighted chemical exchange saturation transfer (gluCEST) MRI provides a non-invasive method for mapping glutamate distribution with high spatial resolution. Collecting data from a large cohort of healthy mice aged 2 to 23 months, scanned in vivo at 17.2 T, we demonstrate that gluCEST can differentiate multiple brain regions, and introduce a gluCEST template for the mouse mid-rostrocaudal brain from Bregma -0.5 to -4 mm approximately. Our findings reveal significant age-related decreases in gluCEST values in the hippocampus, thalamus, and hypothalamus. These decreases did not correlate with volume reductions of these regions, except in the hippocampus, indicating gluCEST as a complementary neuroimaging approach to overall anatomical changes. Our study also demonstrates gluCEST's potential to monitor age-related changes in smaller brain subregions, such as cortical and hippocampal layers, providing a valuable tool for longitudinal investigations into aging and neurodegenerative diseases. The high spatial resolution and sensitivity offered by ultra-high magnetic field MR scanners enhance the precision of these measurements, paving the way for future preclinical and clinical applications.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856118","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":"Correction to: Differential striatal dopamine binding in Parkinson's Disease with and without REM sleep behavior disorder: A Tc‑99 m TRODAT‑1 SPECT study.","authors":"Pei-Hsuan Wang, Yang-Pei Chang, Ching-Fang Chien, Poyin Huang","doi":"10.1007/s11357-026-02301-z","DOIUrl":"https://doi.org/10.1007/s11357-026-02301-z","url":null,"abstract":"","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836506","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":"Epigenetic age acceleration measures and chemotoxicity in older adults with early breast cancer.","authors":"Jingran Ji, Can-Lan Sun, William Dale, Heeyoung Kim, Vani Katheria, Catherine Lee, Claire Smith, Nala Sun, Yuan Chun Ding, Susan L Neuhausen, Harvey J Cohen, Alexandra Binder, Mina S Sedrak","doi":"10.1007/s11357-026-02298-5","DOIUrl":"https://doi.org/10.1007/s11357-026-02298-5","url":null,"abstract":"<p><p>Among older adults with early breast cancer, the risk of chemotoxicity can vary widely despite similar chronological age. Here, we evaluated whether epigenetic indicators of biological age can stratify the risk of chemotoxicity in this population. In a prospective study of 394 women age > 65 with stage I-III breast cancer treated with neo/adjuvant chemotherapy, we analyzed peripheral blood DNA methylation patterns to estimate epigenetic age acceleration (EAA) before chemotherapy. We tested five epigenetic clocks. The primary endpoint was grade 2+ chemotoxicity (yes/no, yes defined as any grade 2+ toxicity attributed to chemotherapy). Using multivariable logistic regression, we examined the association between EAA and grade 2+ chemotoxicity, adjusting for demographic, clinical, and geriatric covariates. We also evaluated the relationship between EAA and individual grade 2+ toxicities. The median (range) pre-treatment chronological age was 70 years (65-85); 65% had stage II/III disease; 38% received anthracycline; and 75% received G-CSF prophylaxis. A total of 334 (84.8%) participants experienced a grade 2+ toxicity. After multivariable adjustment, there was no significant association between measures of EAA and grade 2+ chemotoxicity. For individual toxicities, EAA by GrimAge was associated with increased risk for infection without neutropenia, and EAA by DunedinPACE was associated with increased risk for diarrhea. In this cohort of older adults with early breast cancer, there was no significant association between pre-treatment EAA and overall grade 2+ chemotoxicity. Further research is needed to examine whether blood-based biomarkers of aging may identify older adults at high risk of chemotoxicity. NCT01472094, Hurria Older PatiEnts (HOPE) with Breast Cancer Study.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836709","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":"Plasma pTau181 is associated with subjective cognitive concerns but not objective cognitive decline or structural brain integrity measures in midlife.","authors":"Ashleigh Barrett-Young, Erin E Cawston, Brigid Ryan, Wickliffe C Abraham, Antony Ambler, Tim Anderson, Kirsten Cheyne, Elizabeth Goodin, Sean Hogan, Renate M Houts, David Ireland, Annchen R Knodt, Jesse Kokaua, Tracy R Melzer, Sandhya Ramrakha, Karen Sugden, Benjamin Williams, Phillipa Wilson, Avshalom Caspi, Ahmad R Hariri, Terrie E Moffitt, Richie Poulton, Reremoana Theodore","doi":"10.1007/s11357-026-02282-z","DOIUrl":"https://doi.org/10.1007/s11357-026-02282-z","url":null,"abstract":"<p><p>Although plasma pTau181 has been shown to accurately discriminate patients with Alzheimer's disease from healthy older adults, there are few studies of plasma biomarkers among middle-aged populations. Given the potential utility of plasma AD biomarkers such as pTau181 in screening for disease risk, examining pTau181 in a middle-aged cohort without AD is important for future implementation. The objectives of this study were to characterise plasma pTau181 in a middle-aged birth cohort aged 45 years and to investigate associations with early indicators of dementia risk. Participants were members of the Dunedin Multidisciplinary Health and Development Study, a longitudinal study of 1037 people born in New Zealand in 1972-1973. Plasma pTau181, self-reported cognitive concerns, MRI-based brain structure, and DunedinPACE (an epigenetic biomarker of biological ageing) were measured at age 45; cognition was measured in childhood and age 45. Plasma pTau181 concentrations at age 45 (n = 854, 49% female) were associated with self-reported cognitive concerns (β = 0.09, p = .008); however, no significant associations were observed with objective cognitive decline, worse structural brain integrity, or biological ageing. Higher plasma pTau181 was associated with self-reported cognitive concerns at age 45, but not objective AD-related measures. The association of plasma pTau181 and self-reported cognitive concerns in this cohort suggests that AD pathology may begin to accumulate by age 45 and may be associated with subtle changes in cognition that are not at objectively measurable levels.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837144","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":"Age- and cognitive load-related variability and entropy of gait: integrating coefficient of variation, median absolute deviation, and permutation entropy of spatiotemporal parameters into the Semmelweis Study gait assessment framework.","authors":"Peter Mukli, Mihaly Muranyi, Ágnes Lipecz, Zsofia Szarvas, Tamás Csípő, Mónika Fekete, Vince Fazekas-Pongor, Anna Peterfi, Ágnes Fehér, Norbert Dosa, Csilla Kaposvári, Anna Aliquander, Wei Yi Hung, Dávid Major, Zalan Kaposzta, Attila Matiscsák, Gabriella Dörnyei, Zoltan Benyo, Roland Patai, Boglarka Csík, Rafal Gulej, Anna Ungvari, Panna T Pónyai, Emese Győrffy, Attila Kállai, Márton Sándor, Peter Varga, Adam G Tabak, Stefano Tarantini, Róza Ádány, Béla Merkely, Anna Csiszar, Andriy Yabluchanskiy, Zoltan Ungvari","doi":"10.1007/s11357-026-02256-1","DOIUrl":"https://doi.org/10.1007/s11357-026-02256-1","url":null,"abstract":"<p><p>Aging profoundly alters the neuromotor and cognitive systems that support gait control, leading to increased variability and instability that predict functional decline and dementia risk. In this pilot study, conducted to inform the design of the Semmelweis Study gait assessment pipeline, we examined how aging and cognitive load influence the magnitude and temporal organization of gait fluctuations. The Semmelweis Study is a large, prospective workplace cohort at Semmelweis University designed to identify the determinants of unhealthy aging and the mechanisms that preserve functional resilience across the life course. One hundred three adults aged 23-87 years completed single- and dual-task walking trials on a 20-foot pressure-sensitive walkway. Gait variability was quantified using the median absolute deviation (MAD) and coefficient of variation (CoV) of key spatiotemporal parameters, while permutation entropy (PE) captured the complexity of stride-to-stride dynamics. Aging was associated with progressive increases in both the variability (MAD, CoV) and changes in orderliness (PE) of gait fluctuations, particularly under dual-task conditions, suggesting a dual contribution of neuromotor degradation and compensatory recruitment of higher-order control processes. The amplification of these effects during cognitive load highlights the vulnerability of cognitive-motor integration with advancing age. By integrating robust, relative, and nonlinear variability metrics within a unified analytical framework, this study provides a multidimensional characterization of gait control and establishes sensitive indicators for detecting early functional decline. Within the translational framework of the Semmelweis Study, these quantitative gait measures-together with vascular, metabolic, and cognitive assessments-are expected to serve as informative components of a comprehensive biomarker system aimed at identifying early determinants of unhealthy brain aging and guiding preventive strategies to promote healthy longevity.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836547","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":"Senolytic treatment with dasatinib and quercetin selectively improves cardiac autonomic balance in obesity.","authors":"Mahesh Kumar Sivasubramanian, Raisa Monteiro, Joshua T Butcher, UdayKiran Venugopal, Yasodha Kesavan, Priya Balasubramanian, Madhan Subramanian","doi":"10.1007/s11357-026-02289-6","DOIUrl":"https://doi.org/10.1007/s11357-026-02289-6","url":null,"abstract":"<p><p>Chronic sympathetic nerve activity (SNA) to end organs plays a crucial role in the pathophysiology of obesity-induced hypertension. Oxidative stress and neuroinflammation in the rostral ventrolateral medulla (RVLM), a key brainstem region regulating sympathetic outflow, have been implicated in the sympathetic overactivity in obesity. However, the upstream mechanisms driving RVLM neuroinflammation remain unknown. We hypothesized that obesity induces cellular senescence, a stress response characterized by irreversible cell cycle arrest, in the RVLM and contributes to sympathoexcitation. To test this, C57BL/6 J male mice were fed chow or a high-fat diet (HFD) for 16 weeks, followed by treatment with Dasatinib (5 mg/kg) and Quercetin (50 mg/kg) (D + Q) to selectively eliminate senescent cells. Blood pressure was assessed by radiotelemetry in conscious, freely moving mice. SNA was indirectly measured through heart rate variability (HRV) analysis, depressor response to hexamethonium, and serum norepinephrine levels. The RVLM was microdissected for gene expression and protein analysis of senescence markers and DNA damage. Our results showed that HFD mice had a significant increase in mean arterial pressure and SNA compared to chow-fed controls. Obesity was associated with increased DNA damage and upregulation of cellular senescence markers in the RVLM. Senolytic treatment with D + Q selectively improved cardiac autonomic balance as assessed by HRV, without altering indices of global SNA or blood pressure. Collectively, our findings identify cellular senescence in the RVLM as a novel contributor to obesity-induced sympathoexcitation, and senolytic therapy could be a potential therapeutic avenue for obesity-associated autonomic dysfunction.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837050","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":"Comparative effectiveness of SGLT-2 inhibitors and GLP-1 receptor agonists on the risk of incident dementia after acute kidney injury: a target-trial emulation.","authors":"Ying-Ru Chen, Zheng-Hong Jiang, Jui-Yi Chen, Vin-Cent Wu","doi":"10.1007/s11357-026-02300-0","DOIUrl":"https://doi.org/10.1007/s11357-026-02300-0","url":null,"abstract":"<p><p>Patients with type 2 diabetic mellitus (T2DM) who recover from acute kidney injury (AKI) face substantial risks of cognitive decline and kidney disease progression. Whether sodium-glucosecotransporter-2 inhibitors (SGLT2i) or glucagon-like peptide-1 receptor agonists (GLP-1 RAs) differentially affect incident dementia in this setting is uncertain. We conducted a target trial emulation using TriNetX electronic health records (2015-2024). Adults with T2DM hospitalized for AKI requiring emergent dialysis (AKI-D) were indexed 90 days post-discharge and classified as users of SGLT2i or GLP-1 RAs within that window (intention-to-treat). One-to-one (1:1) propensity score matching (PSM) was performed to control for potential confounding factors. The primary outcome was incident degenerative and vascular dementia. The prespecified secondary outcomes included all-cause mortality, kidney events, and major adverse cardiovascular events (MACE). Among 14,460 eligible patients, SGLT2i users showed a lower risk of degenerative dementia (2.8% vs. 3.9%, aHR 0.78, 95% CI 0.63-0.97; p = 0.028; E value 2.58) and adverse kidney events (7.2% vs. 9.2%, aHR 0.82, 95% CI 0.71-0.95; p = 0.006; E value 2.15) than GLP-1 RAs users. No significant differences were observed for vascular dementia, mortality, or MACE. Safety profiles were similar, with fewer gastrointestinal adverse events in the SGLT2i group. In patients with T2DM recovering from AKI, SGLT2i therapy was associated with reduced risks of degenerative dementia and kidney disease progression compared with GLP-1 RAs. These results suggest that SGLT2i may be a favorable option for cognition during AKI recovery, though further prospective studies are needed to confirm these findings.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836482","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":"A conserved regulatory architecture stabilizes cellular senescence across distinct triggers in human fibroblasts.","authors":"Mohd Shahzaib, Domenico Aprile, Tiziana Squillaro, Nicola Alessio, Gianfranco Peluso, Giovanni Di Bernardo, Umberto Galderisi","doi":"10.1007/s11357-026-02297-6","DOIUrl":"https://doi.org/10.1007/s11357-026-02297-6","url":null,"abstract":"<p><p>Cellular senescence arises through replicative exhaustion or acute stress, yet whether these distinct triggers share a reproducible transcriptional organization has remained unresolved. Seven public human fibroblast RNA-seq datasets were integrated across both trigger types, moving from differential expression through Gene Ontology and Reactome enrichment to protein-protein interaction network embedding within a single harmonized framework. Both triggers converged on concordant repression of replication and chromatin programs alongside induction of inflammatory and extracellular matrix outputs. Cross-trigger combination identified 263 commonly repressed and 112 commonly induced GO terms, with consistently higher enrichment scores in the repressed set, and 145 versus 13 shared Reactome pathways. Conserved induction of calcium ion homeostasis and membrane potential regulation, and conserved repression of RHO GTPase-Formin signaling, extended the shared program beyond canonical SASP biology into dimensions not previously described in human fibroblasts. Interactome embedding, applied here for the first time in a cross-trigger senescence framework, identified ten genes occupying both induced and repressed neighborhoods simultaneously, a structural layer invisible to enrichment analysis alone. ELAVL1 coordinates SASP output and growth arrest post-transcriptionally, while suppressed PARP1 alongside active ATM defines a self-reinforcing damage configuration. These results provide a quantitative cross-study reference and a structured basis for senotherapeutic candidate prioritization.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836501","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":"Loss of sirtuin 3 disrupts cellular senescence signaling pathways.","authors":"Niharika Kura, Bronwyn A Mogck, Samantha T Jezak, Michael C Velarde, Christopher D Wiley","doi":"10.1007/s11357-026-02284-x","DOIUrl":"https://doi.org/10.1007/s11357-026-02284-x","url":null,"abstract":"<p><p>Cellular senescence is a multifaceted stress response marked by stable proliferative arrest and the secretion of diverse biologically active factors, collectively known as the senescence-associated secretory phenotype (SASP). The senescent phenotype is remarkably variable and subject to various regulatory influences. We previously demonstrated that mitochondrial dysfunction induced by diverse stimuli, including the loss of sirtuin 3 (SIRT3), leads to the hyperactivation of AMPK and p53, culminating in senescence while concurrently suppressing much of the proinflammatory SASP. Here, we extend our findings by revealing that the absence of SIRT3 can suppress segments of the SASP even in the absence of p53. Intriguingly, SIRT3 deficiency renders cells resistant to stimulation by exogenous cytokines, such as interleukin-1. Fibroblasts derived from Sirt3 knockout mice exhibit a diminished SASP, including reduced levels of Pdgfa, and these mice display impaired wound healing and a more expansive granulation area. Furthermore, aged Sirt3 knockout mice show disrupted patterns of senescence relative to wild type controls, including increases in senescence markers in adipose tissue, but surprisingly also decreases in liver and heart. Collectively, these data underscore a role for SIRT3 in orchestrating cellular senescence phenotypes, shedding light on its regulatory influence beyond the p53-dependent pathway.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837034","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":"The association between ultra-processed food exposure and cognition in older adults.","authors":"Sarah Gauci, Belayneh Mengist, Mojtaba Lotfaliany, Malcolm Forbes, Farzaneh Asoudeh, Deb Junyi Zhang, Suzanne G Orchard, Alice J Owen, Daniel Clayton-Chubb, Robyn L Woods, John J McNeil, Joanne Ryan, Michael Berk, Adrienne O'Neil, Mohammadreza Mohebbi","doi":"10.1007/s11357-026-02269-w","DOIUrl":"https://doi.org/10.1007/s11357-026-02269-w","url":null,"abstract":"<p><p>With an ageing population comes a growing burden of age-related cognitive decline. While evidence supports a relationship between higher diet quality and better cognitive outcomes, the association between ultra-processed foods (UPFs) and cognitive function remains underexplored. We examined this association using prospective data from the ASPirin in Reducing Events in the Elderly (ASPREE) study, a cohort of Australian adults aged 70 years and older. Dietary intake was assessed via a mail-based diet screening questionnaire and categorised according to the Nova classification. Cognitive performance was assessed using the Controlled Oral Word Association Test (COWAT), Symbol Digit Modalities Test (SDMT), Hopkins Verbal Learning Test-Revised (HVLT-R), Modified Mini-Mental State Examination (3MS), and a composite cognitive Z score. Participants were stratified into high UPF (≥ 4 servings/day) and low UPF (< 4 servings/day). Marginal structural models with inverse probability of treatment weighting estimated associations, adjusting for demographic, lifestyle, and clinical confounders. Among 11,502 participants (3505 high UPF; 7997 low UPF), over a median follow-up of 5.6 (± 2.4) years, higher UPF consumption was associated with poorer performance on the 3MS (mean difference -0.28, 95% CI -0.52 to -0.04), COWAT (-0.23, 95% CI -0.44 to -0.03), SDMT (-0.51, 95% CI -0.94 to -0.08), and the composite Z score (-0.04, 95% CI -0.07 to -0.01), but not HVLT-R (-0.12, 95% CI -0.26 to 0.02). Higher UPF intake was associated with poorer cognitive performance across multiple domains. These findings support initiatives to reduce UPF exposure as a potential strategy to promote healthy cognitive ageing.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837140","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}