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Methods: Fifty-two COLBOS participants completed MMSE, CERAD word memory, grip testing, and MRI/PET for amyloid and tau. Group differences used Mann–Whitney U; correlations used Spearman. Results: Grip strength was similar across mutation status, but carriers showed lower MMSE and higher entorhinal tau PET. Lower grip strength related to greater tau burden in left precuneus. Conclusion: Grip strength may serve as a low-cost marker of tau-related neurodegeneration; larger longitudinal studies are needed.",{"@graph":14,"@context":77},[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/research-report/","Research & 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was the study objective regarding grip strength in ADAD?","Question",{"text":63,"@type":64},"To examine whether handgrip strength was associated with cognition and brain pathology in autosomal dominant Alzheimer’s disease, and whether it differed by PSEN1 E280A mutation status.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"How were participants and outcomes measured?",{"text":68,"@type":64},"The study included 52 COLBOS participants who completed MMSE and CERAD word list memory testing, handgrip dynamometer testing, and MRI/PET imaging for amyloid and tau pathology.",{"name":70,"@type":61,"acceptedAnswer":71},"What were the key findings about handgrip strength and mutation status?",{"text":72,"@type":64},"Handgrip strength did not differ between PSEN1 E280A carriers and non-carriers, and it was not related to age, cognition, or amyloid.",{"name":74,"@type":61,"acceptedAnswer":75},"How did grip strength relate to tau pathology?",{"text":76,"@type":64},"Lower handgrip strength was significantly associated with greater tau burden, particularly in the precuneus of the left hemisphere, supporting its potential as a low-cost marker of tau-related neurodegeneration.","https://schema.org",{"og:url":32,"og:type":79,"og:title":10,"og:site_name":45,"og:description":12},"article",{"robots":81,"canonical":32},"index,follow",{"doc_id":83,"site_id":7},428074,1791292815,{"code":4,"msg":86,"data":87},"success",[88,92,96,100,105,110,115,118,123,126,130],{"id":22,"doc_module":4,"doc_module_name":25,"category_name":89,"show_sort_weight":90,"slug":91},"Story & 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ID: igaf122.3544  \nASSOCIATIONS AMONG HANDGRIP STRENGTH, BRAIN PATHOLOGY, AND COGNITION IN AUTOSOMAL DOMINANT ALZHEIMER’S DISEASE  \nNadeshka Ramirez-Perez1, Ana Baena2, Daniel Vasquez2, Lusiana Martinez1, Averi Giudicessi3, Liliana Ramirez Gomez3, David Aguillon3, and Yakeel Quiroz4, 1. Massachusets General Hospital, Boston, Massachusetts, United States, 2. Universidad de Antioquia, Medellin, Antioquia, Colombia, 3. Massachusetts General Hospital, Boston, Massachusetts, United States,  \n4. Boston University, Boston, Massachusetts, United States  \nObjective: Grip strength decline, and cognitive impairment are prevalent in aging and may reflect shared underlying biological processes. This study examined associations between handgrip strength, brain pathology and cognition in individuals with/without a PSEN1 E280A mutation for autosomal dominant Alzheimer’s disease (ADAD) . We investigated whether handgrip strength differed by mutation status and its association with age and tau pathology. Methods: 52 participants from the Colombia-Boston Biomarker Study (COLBOS) (28 PSEN1-E280A carriers, 24 non-carriers; MAge 34.1 ± 5.5 years; MEducation =9.96 ± 3.94 years; 57.8% female) completed the Mini-Mental State Examination (MMSE), CERAD Word List Memory Test, handgrip test via dynamometer, and MRI and PET imaging for amyloid and tau pathology. Group differences were  \nInnovation in Aging, 2025, Vol. 9, No. S2 1053  \nassessed using Mann–Whitney U tests. Spearman correlations explored associations between handgrip strength, cognition, and PET biomarkers. Results: Handgrip strength did not differ  \nbetween carriers and non-carriers (Carriers: 74.44 +/ - 35.34;  \nnon-carriers: 75.53 +/ - 26.82; p = .62) . Carriers had lower MMSE scores (U = 183.50, p = .004) and greater tau PET burden in the entorhinal cortex (p = .002–.037). Handgrip strength was unrelated to age, cognition or amyloid. Lower handgrip strength was significantly associated with greater tau burden in precuneusin the left hemisphere (ρ = –0.560, p = .019) . Conclusion:  \nAlthough handgrip strength was not linked to carrier status, cognition or amyloid, lower grip strength was associated with greater tau accumulation in the precuneus. These findings highlight handgrip strength as a potential low-cost marker of tau-related neurodegeneration in ADAD. Larger longitudinal studies are needed to extend these results.","cbCaiiIkkaI2HSKf","https://ap.wps.com/l/cbCaiiIkkaI2HSKf","pdf",1799045,"English","# Objective\n# Methods\n# Results\n# Conclusion","[{\"question\":\"What was the study objective regarding grip strength in ADAD?\",\"answer\":\"To examine whether handgrip strength was associated with cognition and brain pathology in autosomal dominant Alzheimer’s disease, and whether it differed by PSEN1 E280A mutation status.\"},{\"question\":\"How were participants and outcomes measured?\",\"answer\":\"The study included 52 COLBOS participants who completed MMSE and CERAD word list memory testing, handgrip dynamometer testing, and MRI/PET imaging for amyloid and tau pathology.\"},{\"question\":\"What were the key findings about handgrip strength and mutation status?\",\"answer\":\"Handgrip strength did not differ between PSEN1 E280A carriers and non-carriers, and it was not related to age, cognition, or amyloid.\"},{\"question\":\"How did grip strength relate to tau pathology?\",\"answer\":\"Lower handgrip strength was significantly associated with greater tau burden, particularly in the precuneus of the left hemisphere, supporting its potential as a low-cost marker of tau-related neurodegeneration.\"}]","ASSOCIATIONS AMONG HANDGRIP STRENGTH, BRAIN PATHOLOGY, AND COGNITION IN AUTOSOMAL DOMINANT ALZHEIMER’S DISEASE - Abstract Citation ID igaf122.3544 | PDF",1790645710]