Etienne Aumont , Marc-André Bedard , Aurélie Bussy , Jaime Fernandez Arias , Cecile Tissot , Brandon J. Hall , Joseph Therriault , Nesrine Rahmouni , Jenna Stevenson , Stijn Servaes , Arthur C. Macedo , Paolo Vitali , Nina Margherita Poltronetti , Olga Fliaguine , Lydia Trudel , Serge Gauthier , Mallar M. Chakravarty , Pedro Rosa-Neto
{"title":"老年人两岁以上海马萎缩与tau蛋白、淀粉样蛋白β和记忆的关系","authors":"Etienne Aumont , Marc-André Bedard , Aurélie Bussy , Jaime Fernandez Arias , Cecile Tissot , Brandon J. Hall , Joseph Therriault , Nesrine Rahmouni , Jenna Stevenson , Stijn Servaes , Arthur C. Macedo , Paolo Vitali , Nina Margherita Poltronetti , Olga Fliaguine , Lydia Trudel , Serge Gauthier , Mallar M. Chakravarty , Pedro Rosa-Neto","doi":"10.1016/j.neurobiolaging.2024.11.007","DOIUrl":null,"url":null,"abstract":"<div><div>In this longitudinal brain imaging study, we aimed to characterize hippocampal tau accumulation and subfield atrophy relative to cortical amyloid-β and memory performance. We measured tau-PET in regions associated with Braak stages I to VI, global amyloid-PET burden, hippocampal subfield volumes and memory assessments from 173 participants aged 55–85. Eighty-six of these participants were tested again two years later. Tau-PET change in the Braak II region, corresponding to the hippocampus and the entorhinal cortex, was significantly associated with the cornu ammonis 1 (CA1) atrophy and memory score. This CA1 atrophy did not significantly mediate the association between tau and memory, nor did global amyloid-PET burden correlate with tau-PET changes in the Braak II region. Longitudinal hippocampal tau accumulation is amyloid-β-independent and co-localized with subfield atrophy. As tau-associated memory decline seems to be independent from hippocampal atrophy, other mechanisms could contribute to the deficit.</div></div>","PeriodicalId":19110,"journal":{"name":"Neurobiology of Aging","volume":"146 ","pages":"Pages 48-57"},"PeriodicalIF":3.7000,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Hippocampal atrophy over two years in relation to tau, amyloid-β and memory in older adults\",\"authors\":\"Etienne Aumont , Marc-André Bedard , Aurélie Bussy , Jaime Fernandez Arias , Cecile Tissot , Brandon J. Hall , Joseph Therriault , Nesrine Rahmouni , Jenna Stevenson , Stijn Servaes , Arthur C. Macedo , Paolo Vitali , Nina Margherita Poltronetti , Olga Fliaguine , Lydia Trudel , Serge Gauthier , Mallar M. Chakravarty , Pedro Rosa-Neto\",\"doi\":\"10.1016/j.neurobiolaging.2024.11.007\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>In this longitudinal brain imaging study, we aimed to characterize hippocampal tau accumulation and subfield atrophy relative to cortical amyloid-β and memory performance. We measured tau-PET in regions associated with Braak stages I to VI, global amyloid-PET burden, hippocampal subfield volumes and memory assessments from 173 participants aged 55–85. Eighty-six of these participants were tested again two years later. Tau-PET change in the Braak II region, corresponding to the hippocampus and the entorhinal cortex, was significantly associated with the cornu ammonis 1 (CA1) atrophy and memory score. This CA1 atrophy did not significantly mediate the association between tau and memory, nor did global amyloid-PET burden correlate with tau-PET changes in the Braak II region. Longitudinal hippocampal tau accumulation is amyloid-β-independent and co-localized with subfield atrophy. As tau-associated memory decline seems to be independent from hippocampal atrophy, other mechanisms could contribute to the deficit.</div></div>\",\"PeriodicalId\":19110,\"journal\":{\"name\":\"Neurobiology of Aging\",\"volume\":\"146 \",\"pages\":\"Pages 48-57\"},\"PeriodicalIF\":3.7000,\"publicationDate\":\"2024-11-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neurobiology of Aging\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0197458024001994\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"GERIATRICS & GERONTOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurobiology of Aging","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0197458024001994","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"GERIATRICS & GERONTOLOGY","Score":null,"Total":0}
Hippocampal atrophy over two years in relation to tau, amyloid-β and memory in older adults
In this longitudinal brain imaging study, we aimed to characterize hippocampal tau accumulation and subfield atrophy relative to cortical amyloid-β and memory performance. We measured tau-PET in regions associated with Braak stages I to VI, global amyloid-PET burden, hippocampal subfield volumes and memory assessments from 173 participants aged 55–85. Eighty-six of these participants were tested again two years later. Tau-PET change in the Braak II region, corresponding to the hippocampus and the entorhinal cortex, was significantly associated with the cornu ammonis 1 (CA1) atrophy and memory score. This CA1 atrophy did not significantly mediate the association between tau and memory, nor did global amyloid-PET burden correlate with tau-PET changes in the Braak II region. Longitudinal hippocampal tau accumulation is amyloid-β-independent and co-localized with subfield atrophy. As tau-associated memory decline seems to be independent from hippocampal atrophy, other mechanisms could contribute to the deficit.
期刊介绍:
Neurobiology of Aging publishes the results of studies in behavior, biochemistry, cell biology, endocrinology, molecular biology, morphology, neurology, neuropathology, pharmacology, physiology and protein chemistry in which the primary emphasis involves mechanisms of nervous system changes with age or diseases associated with age. Reviews and primary research articles are included, occasionally accompanied by open peer commentary. Letters to the Editor and brief communications are also acceptable. Brief reports of highly time-sensitive material are usually treated as rapid communications in which case editorial review is completed within six weeks and publication scheduled for the next available issue.