[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"doc-seo-459436-105":3,"detail-sidebar-cat-0-en-105":81,"doc-detail-459436-en":130},{"code":4,"msg":5,"data":6},0,"ok",{"site_id":7,"language":8,"slug":9,"title":10,"keywords":11,"description":12,"schema_data":13,"social_meta":74,"head_meta":76,"extra_data":78,"updated_unix":80},105,"en","ventricular-remodeling-and-astrocyte-activation-drive-early-protein-aggregation-in-alzheimers-disease-abstract","Ventricular remodeling and astrocyte activation drive early protein aggregation in Alzheimer’s disease - Abstract","","Study findings explain how pro-inflammatory astrocyte activation, choroid plexus dysfunction, and ventricular enlargement may jointly impair cerebrospinal fluid clearance, enabling amyloid-β and tau aggregation in Alzheimer’s disease. Multimodal neuroimaging and fluid biomarkers from 500 TRIAD participants (383 with longitudinal imaging) used structural MRI and PET with [18F]AZD4694 and [18F]MK6240. Reduced ventricular radioactivity, larger ventricular and choroid plexus volumes, and biomarker associations linked amyloid-β burden to ventricular volume and GFAP, with faster cognitive decline in high tertiles of GFAP and ventricular measures.",{"@graph":14,"@context":73},[15,34,56],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/healthcare/","Healthcare",3,{"item":32,"name":10,"@type":21,"position":33},"https://docshare.wps.com/document/ventricular-remodeling-and-astrocyte-activation-drive-early-protein-aggregation-in-alzheimers-disease-abstract/459436/",4,{"url":32,"name":10,"@type":35,"image":36,"author":41,"headline":10,"publisher":44,"fileFormat":47,"inLanguage":8,"description":12,"dateModified":48,"datePublished":49,"encodingFormat":47,"isAccessibleForFree":50,"interactionStatistic":51},"DigitalDocument",{"url":37,"@type":38,"width":39,"height":40},"https://docshare.wps.com/thumbnails/ventricular-remodeling-and-astrocyte-activation-drive-early-protein-aggregation-in-alzheimers-disease-abstract/459436.png","ImageObject",300,407,{"name":42,"@type":43},"Aurelia","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-10-31","2026-09-30",true,{"@type":52,"interactionType":53,"userInteractionCount":55},"InteractionCounter",{"@type":54},"ViewAction",9,{"@type":57,"mainEntity":58},"FAQPage",[59,65,69],{"name":60,"@type":61,"acceptedAnswer":62},"How are ventricular remodeling and astrocyte activation evaluated in this study?","Question",{"text":63,"@type":64},"The study uses multimodal neuroimaging (structural MRI and PET with [18F]AZD4694 for amyloid-β and [18F]MK6240 for tau) plus fluid biomarkers. Ventricular radioactivity proxies choroid plexus function, while plasma GFAP reflects astrocyte activation.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"What key results connect ventricular changes to Alzheimer’s pathology?",{"text":68,"@type":64},"Individuals with amyloid-β and tau pathology show reduced ventricular radioactivity and increased choroid plexus and ventricular volumes. Amyloid-β accumulation associates with ventricular volume and GFAP levels, and larger ventricles with higher amyloid burden correspond to higher tau load.",{"name":70,"@type":61,"acceptedAnswer":71},"Do astrocyte activation and ventricular remodeling act independently according to the conclusion?",{"text":72,"@type":64},"Yes. The conclusion states that astrocyte activation and ventricular remodeling independently contribute to early amyloid-β and tau aggregation. 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Macedo 1  Jaime Fernandez Arias 1  Gleb Bezgin 1   \nKely Monica Quispialaya Socualaya 1  Tevy Chan 1  Yansheng Zheng 1 Serge Gauthier 1  Tharick A Pascoal2  Pedro Rosa-Neto 1  \n1 McGill University, Montreal, QC, Canada  \n2 University of Pittsburgh, Pittsburgh, PA, USA  \nCorrespondence  \nSeyyed Ali Hosseini, McGill University, Montreal, QC, Canada. [Email:](Email: seyyed.ali.hosseini@mail.mcgill.ca)[ seyyed.ali.hosseini@mail.mcgill.ca](Email: seyyed.ali.hosseini@mail.mcgill.ca)  \nAbstract  \nBackground: Pro-inflammatory astrocyte activation, choroid plexus dysfunction, and ventricular enlargement may collectively impair cerebrospinal fluid (CSF) clearance, a process which removes metabolic waste, including amyloid-β and tau. Dysregulated clearance mechanisms may contribute to Alzheimer’s disease pathogenesis (AD) by facilitating protein aggregation. This study investigated whether ventricular remodeling and astrocyte activation drive amyloid-β and tau accumulation in AD. Method: We analyzed multimodal neuroimaging and fluid biomarker data from 500 participants from the Translational Biomarkers in Aging and Dementia (TRIAD) cohort, 383 of whom had longitudinal imaging data (2-4 years follow-up). Structural MRI and PET scans with [18F]AZD4694 (amyloid-β), and [18F]MK6240 (tau) tracers were utilized. Choroid plexus and ventricular volumes were segmented using FreeSurfer and adjusted for intracranial volume. Ventricular radioactivity served as a proxy for choroid plexus function. Plasma glial fibrillary acidic protein (GFAP) levels were used as a biomarker for astrocyte activation. Associations between ventricular remodeling, astrocyte reactivity, and amyloid-β and tau burden were assessed using both region-ofinterest and voxel-wise approaches.  \nResult: We observed significant reductions in ventricular radioactivity, indicative of choroid plexus dysfunction, along with significantly increased choroid plexus and ventricular volumes in individuals with amyloid-β and tau pathology (Figure 1). The [18F]MK6240 time-activity curves in the lateral ventricles highlighted initial peak differences across diagnostic groups (CN (Y), A-T-, A-T+, A+T+), suggesting impaired CSF production and altered choroid plexus function (Figure 1F). Voxel-wise analyses  \nThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.  \n© 2025 The Alzheimer’s Association. Alzheimer’s & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer’s Association.  \nAlzheimer’s Dement. 2025;21(Suppl. 2):e106404.  \n[https://doi.org/10.1002/alz70856_106404](https://doi.org/10.1002/alz70856_106404)  \nwi[leyonlinelibrary.com/journal/alz](leyonlinelibrary.com/journal/alz)  \n1of5  \nBIOMARKERS  \nrevealed that amyloid-β accumulation was significantly associated with ventricular volume and GFAP levels(Figure2). Furthermore, the impact of ventricular enlargement and astrocyte activation on tau accumulation was secondary to amyloid-β (Figure 3), where individuals with larger ventricles and higher amyloid burden exhibited higher tau load (Figure 1c). Kaplan-Meier survival analysis demonstrated that individuals in the highest tertiles of GFAP, ventricular volume, and choroid plexus volume exhibited faster cognitive decline (Figure 1G-J). These effects survived adjustment for amyloid-β and tau loads, without evidence of interaction or mediation.  \nConclusion: Our findings suggest that astrocyte activation and ventricular remodeling independently contribute to early amyloid-β and tau aggregation. E","cbCaipMcoyH0aA3s","https://ap.wps.com/l/cbCaipMcoyH0aA3s","pdf",2963216,"English","# Abstract\n## Background\n## Method\n## Result\n## Conclusion","[{\"question\":\"How are ventricular remodeling and astrocyte activation evaluated in this study?\",\"answer\":\"The study uses multimodal neuroimaging (structural MRI and PET with [18F]AZD4694 for amyloid-β and [18F]MK6240 for tau) plus fluid biomarkers. Ventricular radioactivity proxies choroid plexus function, while plasma GFAP reflects astrocyte activation.\"},{\"question\":\"What key results connect ventricular changes to Alzheimer’s pathology?\",\"answer\":\"Individuals with amyloid-β and tau pathology show reduced ventricular radioactivity and increased choroid plexus and ventricular volumes. Amyloid-β accumulation associates with ventricular volume and GFAP levels, and larger ventricles with higher amyloid burden correspond to higher tau load.\"},{\"question\":\"Do astrocyte activation and ventricular remodeling act independently according to the conclusion?\",\"answer\":\"Yes. The conclusion states that astrocyte activation and ventricular remodeling independently contribute to early amyloid-β and tau aggregation. Elevated GFAP and enlarged ventricles are proposed as biomarkers for accelerated progression risk.\"}]","Ventricular remodeling and astrocyte activation drive early protein aggregation in Alzheimer’s disease - Abstract | PDF",1790755918,13]