Micah J Savin, Haoyang Wang, Heming Pei, Allison E Aiello, Stephanie Assuras, Avshalom Caspi, Terrie E Moffitt, Peter A Muenning, Calen P Ryan, Baoyi Shi, Yaakov Stern, Karen Sugden, Linda Valeri, Daniel W Belsky
{"title":"弗拉明汉心脏研究后代队列中衰老速度表观遗传时钟与认知能力下降率的关系。","authors":"Micah J Savin, Haoyang Wang, Heming Pei, Allison E Aiello, Stephanie Assuras, Avshalom Caspi, Terrie E Moffitt, Peter A Muenning, Calen P Ryan, Baoyi Shi, Yaakov Stern, Karen Sugden, Linda Valeri, Daniel W Belsky","doi":"10.1002/dad2.70038","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>The geroscience hypothesis proposes systemic biological aging is a root cause of cognitive decline.</p><p><strong>Methods: </strong>We analyzed Framingham Heart Study Offspring Cohort data (<i>n</i> = 2296; 46% male; baseline age <i>M </i>= 62, SD = 9, range = 25-101 y). We measured cognitive decline across two decades of neuropsychological-testing follow-up. We measured pace of aging using the DunedinPACE epigenetic clock. Analysis tested if participants with faster DunedinPACE values experienced more rapid cognitive decline compared with those with slower DunedinPACE values.</p><p><strong>Results: </strong>Participants with faster DunedinPACE had poorer cognitive functioning at baseline and experienced more rapid cognitive decline over follow-up. Results were robust to confounders and consistent across population strata. Findings were similar for the PhenoAge and GrimAge epigenetic clocks.</p><p><strong>Discussion: </strong>Faster pace of aging is a risk factor for preclinical cognitive decline. Metrics of biological aging may inform risk stratification in clinical trials and prognosis in patient care.</p><p><strong>Highlights: </strong>Faster DunedinPACE is associated with preclinical cognitive aging.Higher baseline cognition was protective of DunedinPACE-associated cognitive decline.The DunedinPACE association with cognitive decline explained a fourth of dementia risk.</p>","PeriodicalId":53226,"journal":{"name":"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring","volume":"16 4","pages":"e70038"},"PeriodicalIF":4.0000,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11585167/pdf/","citationCount":"0","resultStr":"{\"title\":\"Association of a pace of aging epigenetic clock with rate of cognitive decline in the Framingham Heart Study Offspring Cohort.\",\"authors\":\"Micah J Savin, Haoyang Wang, Heming Pei, Allison E Aiello, Stephanie Assuras, Avshalom Caspi, Terrie E Moffitt, Peter A Muenning, Calen P Ryan, Baoyi Shi, Yaakov Stern, Karen Sugden, Linda Valeri, Daniel W Belsky\",\"doi\":\"10.1002/dad2.70038\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>The geroscience hypothesis proposes systemic biological aging is a root cause of cognitive decline.</p><p><strong>Methods: </strong>We analyzed Framingham Heart Study Offspring Cohort data (<i>n</i> = 2296; 46% male; baseline age <i>M </i>= 62, SD = 9, range = 25-101 y). We measured cognitive decline across two decades of neuropsychological-testing follow-up. We measured pace of aging using the DunedinPACE epigenetic clock. Analysis tested if participants with faster DunedinPACE values experienced more rapid cognitive decline compared with those with slower DunedinPACE values.</p><p><strong>Results: </strong>Participants with faster DunedinPACE had poorer cognitive functioning at baseline and experienced more rapid cognitive decline over follow-up. Results were robust to confounders and consistent across population strata. Findings were similar for the PhenoAge and GrimAge epigenetic clocks.</p><p><strong>Discussion: </strong>Faster pace of aging is a risk factor for preclinical cognitive decline. Metrics of biological aging may inform risk stratification in clinical trials and prognosis in patient care.</p><p><strong>Highlights: </strong>Faster DunedinPACE is associated with preclinical cognitive aging.Higher baseline cognition was protective of DunedinPACE-associated cognitive decline.The DunedinPACE association with cognitive decline explained a fourth of dementia risk.</p>\",\"PeriodicalId\":53226,\"journal\":{\"name\":\"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring\",\"volume\":\"16 4\",\"pages\":\"e70038\"},\"PeriodicalIF\":4.0000,\"publicationDate\":\"2024-11-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11585167/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1002/dad2.70038\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/10/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q1\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/dad2.70038","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/10/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
Association of a pace of aging epigenetic clock with rate of cognitive decline in the Framingham Heart Study Offspring Cohort.
Introduction: The geroscience hypothesis proposes systemic biological aging is a root cause of cognitive decline.
Methods: We analyzed Framingham Heart Study Offspring Cohort data (n = 2296; 46% male; baseline age M = 62, SD = 9, range = 25-101 y). We measured cognitive decline across two decades of neuropsychological-testing follow-up. We measured pace of aging using the DunedinPACE epigenetic clock. Analysis tested if participants with faster DunedinPACE values experienced more rapid cognitive decline compared with those with slower DunedinPACE values.
Results: Participants with faster DunedinPACE had poorer cognitive functioning at baseline and experienced more rapid cognitive decline over follow-up. Results were robust to confounders and consistent across population strata. Findings were similar for the PhenoAge and GrimAge epigenetic clocks.
Discussion: Faster pace of aging is a risk factor for preclinical cognitive decline. Metrics of biological aging may inform risk stratification in clinical trials and prognosis in patient care.
Highlights: Faster DunedinPACE is associated with preclinical cognitive aging.Higher baseline cognition was protective of DunedinPACE-associated cognitive decline.The DunedinPACE association with cognitive decline explained a fourth of dementia risk.
期刊介绍：
Alzheimer''s & Dementia: Diagnosis, Assessment & Disease Monitoring (DADM) is an open access, peer-reviewed, journal from the Alzheimer''s Association® that will publish new research that reports the discovery, development and validation of instruments, technologies, algorithms, and innovative processes. Papers will cover a range of topics interested in the early and accurate detection of individuals with memory complaints and/or among asymptomatic individuals at elevated risk for various forms of memory disorders. The expectation for published papers will be to translate fundamental knowledge about the neurobiology of the disease into practical reports that describe both the conceptual and methodological aspects of the submitted scientific inquiry. Published topics will explore the development of biomarkers, surrogate markers, and conceptual/methodological challenges. Publication priority will be given to papers that 1) describe putative surrogate markers that accurately track disease progression, 2) biomarkers that fulfill international regulatory requirements, 3) reports from large, well-characterized population-based cohorts that comprise the heterogeneity and diversity of asymptomatic individuals and 4) algorithmic development that considers multi-marker arrays (e.g., integrated-omics, genetics, biofluids, imaging, etc.) and advanced computational analytics and technologies.
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