Alzheimer's & Dementia最新文献

{"title":"Accelerated ovarian failure results in brain alterations related to Alzheimer's disease that are not recovered by high-intensity interval training in mice","authors":"Ahmad Mohammad, Michael S. Finch, Sarah Rouhana, Parastoo Mashouri, Ciara Barry, Emma F. Hubbard, Newman Sze, Shawn M. Beaudette, W. Glen Pyle, Geoffrey A. Power, Rebecca E. K. MacPherson","doi":"10.1002/alz.14463","DOIUrl":"https://doi.org/10.1002/alz.14463","url":null,"abstract":"The menopausal decline in ovarian estrogen production is thought to increase the risk of Alzheimer's disease; however, this link requires further investigation. The chronological development of this connection is not well defined because of the lack of animal models that recapitulate the time course of menopause. This study characterized the cognitive and neuronal effects of the 4-vinylcyclohexene diepoxide (VCD) model of ovarian failure in female mice and assessed whether high-intensity interval training (HIIT) would attenuate impairments.","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"92 1","pages":""},"PeriodicalIF":14.0,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142874184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TMEM106B C‐terminal fragments aggregate and drive neurodegenerative proteinopathy in transgenic Caenorhabditis elegans","authors":"Ruben Riordan, Aleen Saxton, Marina Han, Pamela J. McMillan, Rebecca L. Kow, Nicole F. Liachko, Brian C. Kraemer","doi":"10.1002/alz.14468","DOIUrl":"https://doi.org/10.1002/alz.14468","url":null,"abstract":"INTRODUCTIONGenetic variation in the lysosomal and transmembrane protein 106B (TMEM106B) modifies risk for several neurodegenerative disorders, especially frontotemporal lobar degeneration (FTLD). The C‐terminal (CT) domain of TMEM106B occurs as fibrillar protein deposits in the brains of dementia patients.METHODSTo determine the TMEM CT aggregation propensity and neurodegenerative potential, we generated transgenic <jats:italic>Caenorhabditis elegans</jats:italic> expressing the human TMEM CT fragment aggregating in FTLD cases.RESULTSPan‐neuronal expression of human TMEM CT in <jats:italic>C. elegans</jats:italic> causes severe neuronal dysfunction driving neurodegeneration. Cytosolic aggregation of TMEM CT proteins accompanied by behavioral dysfunction and neurodegeneration. Loss of <jats:italic>pgrn‐1</jats:italic> did not modify TMEM CT phenotypes suggesting TMEM CT aggregation occurs downstream of PGRN loss of function. The mechanistic drivers of TMEM106B proteinopathy appear distinct from known modifiers of tauopathy.DISCUSSIONOur data demonstrate that TMEM CT aggregation can kill neurons. TMEM106B transgenic <jats:italic>C.elegans</jats:italic> provide a useful model for characterizing TMEM106B proteinopathy‐mediated neurodegeneration in FTLD.Highlights<jats:list list-type=\"bullet\"> <jats:list-item>Pan‐neuronal expression of human TMEM106B C‐terminal fragments (TMEM CT) in <jats:italic>C. elegans</jats:italic> neurons drives a suite of disease‐related phenotypes useful for modeling the molecular and cellular features of TMEM106B neuropathology.</jats:list-item> <jats:list-item>TMEM CT expression results in extensive TMEM aggregation and accumulation of highly detergent insoluble protein species.</jats:list-item> <jats:list-item>TMEM CT expression causes moderate to severe neuronal dysfunction dependent on TMEM CT abundance as measured by stereotypical behavioral readouts.</jats:list-item> <jats:list-item>TMEM CT expression drives significant neurodegenerative changes.</jats:list-item> <jats:list-item>Dendra2 tagged TMEM exhibits similar properties to untagged TMEM allowing ready visualization of the protein.</jats:list-item> <jats:list-item>TMEM CT aggregates accumulate adjacent to but not within lysosomes.</jats:list-item> <jats:list-item>PGRN loss of function does not impact TMEM CT toxicity.</jats:list-item> <jats:list-item>Modifiers of tau and TDP‐43 proteinopathies have little impact on TMEM CT‐related neurodegenerative phenotypes.</jats:list-item> </jats:list>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"32 1","pages":""},"PeriodicalIF":14.0,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142874190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alzheimer's Association clinical practice guideline for the Diagnostic Evaluation, Testing, Counseling, and Disclosure of Suspected Alzheimer's Disease and Related Disorders (DETeCD‐ADRD): Executive summary of recommendations for primary care","authors":"Alireza Atri, Bradford C. Dickerson, Carolyn Clevenger, Jason Karlawish, David Knopman, Pei‐Jung Lin, Mary Norman, Chiadi Onyike, Mary Sano, Susan Scanland, Maria Carrillo","doi":"10.1002/alz.14333","DOIUrl":"https://doi.org/10.1002/alz.14333","url":null,"abstract":"<jats:label/>US clinical practice guidelines for the diagnostic evaluation of cognitive impairment due to Alzheimer's disease (AD) or AD and related dementias (ADRD) are decades old and aimed at specialists. This evidence‐based guideline was developed to empower all—including primary care—clinicians to implement a structured approach for evaluating a patient with symptoms that may represent clinical AD/ADRD. Through a modified‐Delphi approach and guideline‐development process (7374 publications were reviewed; 133 met inclusion criteria) an expert workgroup developed recommendations as steps in a patient‐centered evaluation process. This summary focuses on recommendations, appropriate for any practice setting, forming core elements of a high‐quality, evidence‐supported evaluation process aimed at characterizing, diagnosing, and disclosing the patient's cognitive functional status, cognitive–behavioral syndrome, and likely underlying brain disease so that optimal care plans to maximize patient/care partner dyad quality of life can be developed; a companion article summarizes specialist recommendations. If clinicians use this guideline and health‐care systems provide adequate resources, outcomes should improve in most patients in most practice settings.Highlights<jats:list list-type=\"bullet\"> <jats:list-item>US clinical practice guidelines for the diagnostic evaluation of cognitive impairment due to Alzheimer's disease (AD) or AD and related dementias (ADRD) are decades old and aimed at specialists.</jats:list-item> <jats:list-item>This evidence‐based guideline was developed to empower all—including primary care—clinicians to implement a structured approach for evaluating a patient with symptoms that may represent clinical AD/ADRD.</jats:list-item> <jats:list-item>This summary focuses on recommendations, appropriate for any practice setting, forming core elements of a high‐quality, evidence‐supported evaluation process aimed at characterizing, diagnosing, and disclosing the patient's cognitive functional status, cognitive–behavioral syndrome, and likely underlying brain disease so that optimal care plans to maximize patient/care partner dyad quality of life can be developed; a companion article summarizes specialist recommendations.</jats:list-item> <jats:list-item>If clinicians use this guideline and health‐care systems provide adequate resources, outcomes should improve in most patients in most practice settings.</jats:list-item></jats:list>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"13 1","pages":""},"PeriodicalIF":14.0,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142874194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alzheimer's Association's funding portfolio: Insights from the International Alzheimer's and Related Dementias Research Portfolio (IADRP)","authors":"Courtney M. Kloske, Stefania Forner, Emily A. Meyers, Albert E. Towers, Heather M. Snyder, Maria C. Carrillo","doi":"10.1002/alz.14354","DOIUrl":"https://doi.org/10.1002/alz.14354","url":null,"abstract":"INTRODUCTIONAlzheimer's disease (AD) and related dementias (ADRD) present significant health challenges. Understanding their underlying biology, advancing existing and new therapies, and enhancing care for patients and caregivers are critical priorities.METHODSThis article utilizes data from the International Alzheimer's and Related Dementias Research Portfolio (IADRP) to analyze funding patterns from the Alzheimer's Association over the past decade.RESULTSAs the largest nonprofit funder of AD/ADRD research globally, the Alzheimer's Association has committed over $430 million, supporting a diverse range of studies across the entire spectrum of dementia‐related science. The funding landscape has evolved, reflecting new areas of investigation and collaboration with broader research initiatives.DISCUSSIONThis article highlights the dynamic nature of the Association's funding strategies and ongoing efforts to connect funding with additional supportive resources, thereby enhancing the overall research ecosystemHighlights<jats:list list-type=\"bullet\"> <jats:list-item>As the world's largest nonprofit funder of Alzheimer's disease and dementia science, the Alzheimer's Association's funding activities are strategically designed in partnership with the global research community to address scientific gaps in our knowledge to advance research.</jats:list-item> <jats:list-item>A large part of the Association's funding portfolio depends on key partnerships and collaborations.</jats:list-item> <jats:list-item>From 2019 to 2023, the Alzheimer's Association has allocated funding for more than 850 new research studies. The diversity of areas funded is clear across the Association's portfolio.</jats:list-item> <jats:list-item>Beyond the Association's strong emphasis on supporting research through grant funding, there are also efforts to ensure the necessary ecosystem to support the career development of researchers and clinicians, maintaining ongoing support for current and future awardees, including convening and the Alzheimer's Association International Society to Advance Alzheimer's Research and Treatment (ISTAART).</jats:list-item></jats:list>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"60 1","pages":""},"PeriodicalIF":14.0,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142874262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stabilization of mitochondria‐associated endoplasmic reticulum membranes regulates Aβ generation in a three‐dimensional neural model of Alzheimer's disease","authors":"Jacob C. Zellmer, Marina B. Tarantino, Michelle Kim, Selene Lomoio, Masato Maesako, György Hajnóczky, Raja Bhattacharyya","doi":"10.1002/alz.14417","DOIUrl":"https://doi.org/10.1002/alz.14417","url":null,"abstract":"INTRODUCTIONWe previously demonstrated that regulating mitochondria‐associated endoplasmic reticulum (ER) membranes (MAMs) affects axonal Aβ generation in a well‐characterized three‐dimensional (3D) neural Alzheimer's disease (AD) model. MAMs vary in thickness and length, impacting their functions. Here, we examined the effect of MAM thickness on Aβ in our 3D neural model of AD.METHODSWe employed fluorescence resonance energy transfer (FRET) or fluorescence‐based MAM stabilizers, electron microscopy, Aβ enzyme‐linked immunosorbent assay (ELISA), and live‐cell imaging with kymography to assess how stabilizing MAMs of different gap widths influence Aβ production and MAM axonal mobility.RESULTSStabilizing tight MAMs (∼6 nm gap width) significantly increased Aβ levels, whereas basal (∼25 nm) and loose MAMs (∼40 nm) maintained or reduced Aβ levels, respectively. Tight MAMs reduced mitochondrial axonal velocity compared to basal MAMs, while loose MAMs showed severely reduced axonal distribution.DISCUSSIONOur findings suggest that stabilizing MAMs of specific gap widths, particularly in axons, without complete destabilization could be an effective therapeutic strategy for AD.Highlights<jats:list list-type=\"bullet\"> <jats:list-item>The stabilization of MAMs exacerbates or ameliorates Aβ generation from AD neurons in a MAM gap width‐dependent manner.</jats:list-item> <jats:list-item>A specific stabilization threshold within the MAM gap width spectrum shifts the amyloidogenic process to non‐amyloidogenic.</jats:list-item> <jats:list-item>Tight MAMs slow down mitochondrial axonal transport compared to lose MAMs offering a quantitative method for measuring MAM stabilization.</jats:list-item> </jats:list>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"13 1","pages":""},"PeriodicalIF":14.0,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142874627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A whole-brain functional connectivity model of Alzheimer's disease pathology","authors":"Ruchika S. Prakash, Michael R. McKenna, Oyetunde Gbadeyan, Anita R. Shankar, Erika A. Pugh, James Teng, Rebecca Andridge, Anne Berry, Douglas W. Scharre","doi":"10.1002/alz.14349","DOIUrl":"https://doi.org/10.1002/alz.14349","url":null,"abstract":"Alzheimer's disease (AD) is characterized by the presence of two proteinopathies, amyloid and tau, which have a cascading effect on the functional and structural organization of the brain.","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"123 1","pages":""},"PeriodicalIF":14.0,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142873947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differences in baseline cognitive performance between participants with early-onset and late-onset Alzheimer's disease: Comparison of LEADS and ADNI","authors":"Dustin B. Hammers, Ani Eloyan, Maryanne Thangarajah, Alexander Taurone, Laurel Beckett, Sujuan Gao, Angelina J. Polsinelli, Kala Kirby, Jeffrey L. Dage, Kelly Nudelman, Paul Aisen, Rema Reman, Renaud La Joie, Julien Lagarde, Alireza Atri, David Clark, Gregory S. Day, Ranjan Duara, Neill R. Graff-Radford, Lawrence S. Honig, David T. Jones, Joseph C. Masdeu, Mario F. Mendez, Kyle Womack, Erik Musiek, Chiadi U. Onyike, Meghan Riddle, Ian Grant, Emily Rogalski, Erik C. B. Johnson, Steven Salloway, Sharon J. Sha, Raymond Scott Turner, Thomas S. Wingo, David A. Wolk, Maria C. Carrillo, Bradford C. Dickerson, Gil D. Rabinovici, Liana G. Apostolova","doi":"10.1002/alz.14218","DOIUrl":"https://doi.org/10.1002/alz.14218","url":null,"abstract":"Early-onset Alzheimer's disease (EOAD) and late-onset Alzheimer's disease (LOAD) share similar amyloid etiology, but evidence from smaller-scale studies suggests that they manifest differently clinically. Current analyses sought to contrast the cognitive profiles of EOAD and LOAD.","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"1 1","pages":""},"PeriodicalIF":14.0,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142873951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sodium-glucose cotransporter-2 inhibitors use and risk of dementia in different ethnoracial groups with type 2 diabetes","authors":"Shih-Chi Yang, Wen-Chieh Liao, Yi-Sheng Jhang, Hui-Chin Chang, Yu-Jung Su, Shiu-Jau Chen, Shuo-Yan Gau","doi":"10.1002/alz.14353","DOIUrl":"https://doi.org/10.1002/alz.14353","url":null,"abstract":"&lt;p&gt;Dear Editor,&lt;/p&gt;\u0000&lt;p&gt;The link between dementia and glucose-lowering drugs has been widely studied. Tang et al. reported that new users of sodium-glucose cotransporter-2 (SGLT2) inhibitors had a lower risk of dementia compared to sulfonylurea users.&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt; Other glucose-lowering drugs, like metformin and glucagon-like peptide-1 (GLP-1) receptor agonists (GLP-1RAs), are also associated with reduced dementia risk and slower cognitive decline in type 2 diabetes patients. Previous studies used various glucose-lowering drugs as active comparators to assess SGLT-2 inhibitors' effects on dementia.&lt;span&gt;&lt;sup&gt;2, 3&lt;/sup&gt;&lt;/span&gt; However, studies have shown significant ethnoracial disparities in dementia, with Black individuals (compared to White individuals) and Hispanic individuals (compared to non-Hispanic, predominantly White individuals) experiencing higher prevalence and incidence rates of dementia.&lt;span&gt;&lt;sup&gt;4, 5&lt;/sup&gt;&lt;/span&gt; Moreover, both Black and Hispanic populations are at a greater risk of developing type 2 diabetes, which is itself a known risk factor for dementia. Ensuring that these at-risk ethnoracial groups can access and benefit from targeted interventions is therefore essential for promoting brain health equity. To address the knowledge gap, we hereby conducted an analysis using the TriNetX research network, which has not been fully explored in previous studies.&lt;span&gt;&lt;sup&gt;6, 7&lt;/sup&gt;&lt;/span&gt;&lt;/p&gt;\u0000&lt;p&gt;We utilized the TriNetX research network, specifically the US Collaborative Network subset, which includes 66 US institutions and is updated monthly, and applied in various epidemiological studies.&lt;span&gt;&lt;sup&gt;8, 9&lt;/sup&gt;&lt;/span&gt; It offers access to anonymized electronic medical records and claims data, including patient information from healthcare organizations (HCOs) related to disease diagnoses, medication prescriptions, medical procedures, and laboratory results. Participants were aged 50 years and older, diagnosed with diabetes mellitus between January 1, 2018, and December 31, 2021, and had more than two visit records. The control group included diabetes patients using sulfonylureas, metformin, dipeptidyl peptidase-4 (DPP4) inhibitors, and GLP-1 RAs. Exclusions were made for those under 50; those with prior dementia, Parkinson's disease, or Alzheimer's disease; or those who were deceased before the index date. The case group consisted of SGLT-2 users. Individuals who had ever used the alternate drug were excluded when comparing the two drug groups. Before matching and exclusion of prior glucose-lowering drug use, there were 279,122 SGLT-2 inhibitor users, 512,944 sulfonylurea users, 1,301,591 metformin users, 319,098 DPP4 inhibitor users, and 306,499 GLP-1 RA users. A 1:1 propensity score matching was performed in all analyses. 1:1 ratio. The primary outcome was new-onset dementia, with participants monitored from 3 months post-index date until dementia occurrence or their last visit, whichever came first. To assess potential","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"32 1","pages":""},"PeriodicalIF":14.0,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142873952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diagnostic accuracy of phosphorylated tau217 in detecting Alzheimer's disease pathology among cognitively impaired and unimpaired: A systematic review and meta-analysis","authors":"Mohammad Khalafi, William J. Dartora, Laura Beth J. McIntire, Tracy A. Butler, Krista M. Wartchow, Seyed Hani Hojjati, Qolamreza R. Razlighi, Kiarash Shirbandi, Liangdong Zhou, Kewei Chen, Ke Xi, Samprit Banerjee, Nancy Foldi, Silky Pahlajani, Lidia Glodzik, Yi Li, Mony J. de Leon, Gloria C. Chiang","doi":"10.1002/alz.14458","DOIUrl":"https://doi.org/10.1002/alz.14458","url":null,"abstract":"Our review summarizes the diagnostic accuracy of plasma and cerebrospinal fluid (CSF) phosphorylated tau 217 (p-tau217) in detecting amyloid and tau pathology on positron emission tomography (PET). We systematically reviewed studies that reported the diagnostic accuracy of plasma and CSF p-tau217, searching MEDLINE/PubMed, Scopus, and Web of Science through August 2024. The accuracy of p-tau217 in predicting amyloid and tau pathology on PET was evaluated in 30 studies. Both plasma and CSF p-tau217 effectively detect amyloid and tau PET deposition. Plasma p-tau217 showed 82% sensitivity for detecting amyloid and 83% for tau, with 86% and 83% specificity, respectively. CSF p-tau217 had 79% sensitivity for amyloid and 91% for tau, with 91% and 84% specificity. p-tau217 effectively identifies Alzheimer's disease (AD) pathology. Plasma p-tau217 was comparable to CSF p-tau217 in detecting amyloid deposition on PET. Despite being less sensitive for detecting tau deposition on PET, plasma p-tau217 can be an efficient screening tool for underlying AD pathology.","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"128 1","pages":""},"PeriodicalIF":14.0,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142874177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Life's Essential 8 and midlife trajectories in cognition and brain health: The CARDIA study","authors":"Christina Silvia Dintica, Xiaqing Jiang, Lenore J. Launer, R. Nick Bryan, Kristine Yaffe","doi":"10.1002/alz.14464","DOIUrl":"https://doi.org/10.1002/alz.14464","url":null,"abstract":"Poor cardiovascular health (CVH) is linked to Alzheimer's disease and dementia; however, its association with neurocognitive trajectories earlier in life remains underexplored.","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"17 1","pages":""},"PeriodicalIF":14.0,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142874179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}