{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T18:36:17Z","timestamp":1791311777921,"version":"4.3.1"},"reference-count":56,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2013,4,9]],"date-time":"2013-04-09T00:00:00Z","timestamp":1365465600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["K99AG031293"],"award-info":[{"award-number":["K99AG031293"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01NS33249"],"award-info":[{"award-number":["R01NS33249"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["P30AG10161"],"award-info":[{"award-number":["P30AG10161"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01AG15819"],"award-info":[{"award-number":["R01AG15819"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2013,5,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Alzheimer\u2019s disease begins about two decades before the onset of symptoms or neuron death, and is believed to be caused by pathogenic amyloid-\u03b2 aggregates that initiate a cascade of molecular events culminating in widespread neurodegeneration. The microtubule binding protein tau may mediate the effects of amyloid-\u03b2 in this cascade. Amyloid plaques comprised of insoluble, fibrillar amyloid-\u03b2 aggregates are the most characteristic feature of Alzheimer\u2019s disease. However, the correspondence between the distribution of plaques and the pattern of neurodegeneration is tenuous. This discrepancy has stimulated the investigation of other amyloid-\u03b2 aggregates, including soluble amyloid-\u03b2 oligomers. Different soluble amyloid-\u03b2 oligomers have been studied in several mouse models, but not systematically in humans. Here, we measured three amyloid-\u03b2 oligomers previously described in mouse models\u2014amyloid-\u03b2 trimers, A\u03b2*56 and amyloid-\u03b2 dimers\u2014in brain tissue from 75 cognitively intact individuals, ranging from young children to the elderly, and 58 impaired subjects with mild cognitive impairment or probable Alzheimer\u2019s disease. As in mouse models, where amyloid-\u03b2 trimers appear to be the fundamental amyloid-\u03b2 assembly unit of A\u03b2*56 and are present in young mice prior to memory decline, amyloid-\u03b2 trimers in humans were present in children and adolescents; their levels rose gradually with age and were significantly above baseline in subjects in their 70s. A\u03b2*56 levels were negligible in children and young adults, rose significantly above baseline in subjects in their 40s and increased steadily thereafter. Amyloid-\u03b2 dimers were undetectable until subjects were in their 60s; their levels then increased sharply and correlated with plaque load. Remarkably, in cognitively intact individuals we found strong positive correlations between A\u03b2*56 and two pathological forms of soluble tau (tau-CP13 and tau-Alz50), and negative correlations between A\u03b2*56 and two postsynaptic proteins (drebrin and fyn kinase), but none between amyloid-\u03b2 dimers or amyloid-\u03b2 trimers and tau or synaptic proteins. Comparing impaired with age-matched unimpaired subjects, we found the highest levels of amyloid-\u03b2 dimers, but the lowest levels of A\u03b2*56 and amyloid-\u03b2 trimers, in subjects with probable Alzheimer\u2019s disease. In conclusion, in cognitively normal adults A\u03b2*56 increased ahead of amyloid-\u03b2 dimers or amyloid-\u03b2 trimers, and pathological tau proteins and postsynaptic proteins correlated with A\u03b2*56, but not amyloid-\u03b2 dimers or amyloid-\u03b2 trimers. We propose that A\u03b2*56 may play a pathogenic role very early in the pathogenesis of Alzheimer\u2019s disease.<\/jats:p>","DOI":"10.1093\/brain\/awt062","type":"journal-article","created":{"date-parts":[[2013,4,10]],"date-time":"2013-04-10T20:29:59Z","timestamp":1365625799000},"page":"1383-1398","source":"Crossref","is-referenced-by-count":391,"title":["Brain amyloid-\u03b2 oligomers in ageing and Alzheimer\u2019s disease"],"prefix":"10.1093","volume":"136","author":[{"given":"Sylvain E.","family":"Lesn\u00e9","sequence":"first","affiliation":[{"name":"1 1 Department of Neuroscience, University of Minnesota, Minneapolis, MN 55455 USA"},{"name":"2 2 N. Bud Grossman Centre for Memory Research and Care, University of Minnesota, Minneapolis, MN 55455 USA"},{"name":"3 3 Institute for Translational Neuroscience, University of Minnesota, Minneapolis, MN 55455 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mathew A.","family":"Sherman","sequence":"additional","affiliation":[{"name":"1 1 Department of Neuroscience, University of Minnesota, Minneapolis, MN 55455 USA"},{"name":"2 2 N. Bud Grossman Centre for Memory Research and Care, University of Minnesota, Minneapolis, MN 55455 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marianne","family":"Grant","sequence":"additional","affiliation":[{"name":"2 2 N. Bud Grossman Centre for Memory Research and Care, University of Minnesota, Minneapolis, MN 55455 USA"},{"name":"4 4 Department of Neurology, University of Minnesota, Minneapolis, MN 55455 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Kuskowski","sequence":"additional","affiliation":[{"name":"5 5 Rush Alzheimer\u2019s Disease Centre, Rush University Medical Centre, Chicago, IL 60612 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie A.","family":"Schneider","sequence":"additional","affiliation":[{"name":"5 5 Rush Alzheimer\u2019s Disease Centre, Rush University Medical Centre, Chicago, IL 60612 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David A.","family":"Bennett","sequence":"additional","affiliation":[{"name":"5 5 Rush Alzheimer\u2019s Disease Centre, Rush University Medical Centre, Chicago, IL 60612 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karen H.","family":"Ashe","sequence":"additional","affiliation":[{"name":"2 2 N. Bud Grossman Centre for Memory Research and Care, University of Minnesota, Minneapolis, MN 55455 USA"},{"name":"3 3 Institute for Translational Neuroscience, University of Minnesota, Minneapolis, MN 55455 USA"},{"name":"4 4 Department of Neurology, University of Minnesota, Minneapolis, MN 55455 USA"},{"name":"6 6 Geriatric Research Education Clinical Centre, VA Medical Centre, Minneapolis, MN 55417 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2013,4,9]]},"reference":[{"key":"2024110407435006800_awt062-B1","doi-asserted-by":"crossref","first-page":"492","DOI":"10.1002\/ana.21509","article-title":"Prodromal Alzheimer's disease: successive emergence of the clinical symptoms","volume":"64","author":"Amieva","year":"2008","journal-title":"Ann Neurol"},{"key":"2024110407435006800_awt062-B2","doi-asserted-by":"crossref","first-page":"631","DOI":"10.1016\/j.neuron.2010.04.031","article-title":"Probing the biology of Alzheimer's 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