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dc.contributor.authorMcCarter, Joanna F.en_US
dc.contributor.authorLiebscher, Sabineen_US
dc.contributor.authorBachhuber, Teresaen_US
dc.contributor.authorAbou-Ajram, Claudiaen_US
dc.contributor.authorHübener, Marken_US
dc.contributor.authorHyman, Bradley T.en_US
dc.contributor.authorHaass, Christianen_US
dc.contributor.authorMeyer-Luehmann, Melanieen_US
dc.date.accessioned2014-02-18T18:11:46Z
dc.date.issued2013en_US
dc.identifier.citationMcCarter, Joanna F., Sabine Liebscher, Teresa Bachhuber, Claudia Abou-Ajram, Mark Hübener, Bradley T. Hyman, Christian Haass, and Melanie Meyer-Luehmann. 2013. “Clustering of plaques contributes to plaque growth in a mouse model of Alzheimer’s disease.” Acta Neuropathologica 126 (2): 179-188. doi:10.1007/s00401-013-1137-2. http://dx.doi.org/10.1007/s00401-013-1137-2.en
dc.identifier.issn0001-6322en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:11717622
dc.description.abstractAmyloid-β (Aβ) plaque deposition plays a central role in the pathogenesis of Alzheimer’s disease (AD). Post-mortem analysis of plaque development in mouse models of AD revealed that plaques are initially small, but then increase in size and become more numerous with age. There is evidence that plaques can grow uniformly over time; however, a complementary hypothesis of plaque development is that small plaques cluster and grow together thereby forming larger plaques. To investigate the latter hypothesis, we studied plaque formation in APPPS1 mice using in vivo two-photon microscopy and immunohistochemical analysis. We used sequential pre- and post-mortem staining techniques to label plaques at different stages of development and to detect newly emerged plaques. Post-mortem analysis revealed that a subset (22 %) of newly formed plaques appeared very close (<40 μm) to pre-existing plaques and that many close plaques (25 %) that were initially separate merged over time to form one single large plaque. Our results suggest that small plaques can cluster together, thus forming larger plaques as a complementary mechanism to simple uniform plaque growth from a single initial plaque. This study deepens our understanding of Aβ deposition and demonstrates that there are multiple mechanisms at play in plaque development. Electronic supplementary material The online version of this article (doi:10.1007/s00401-013-1137-2) contains supplementary material, which is available to authorized users.en
dc.language.isoen_USen
dc.publisherSpringer Berlin Heidelbergen
dc.relation.isversionofdoi:10.1007/s00401-013-1137-2en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3722456/pdf/en
dash.licenseLAAen_US
dc.subjectAlzheimer’s diseaseen
dc.subjectAmyloid plaquesen
dc.subjectAPPPS1 transgenic miceen
dc.subjectTwo-photon in vivo imagingen
dc.titleClustering of plaques contributes to plaque growth in a mouse model of Alzheimer’s diseaseen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalActa Neuropathologicaen
dash.depositing.authorHyman, Bradley T.en_US
dc.date.available2014-02-18T18:11:46Z
dc.identifier.doi10.1007/s00401-013-1137-2*
dash.contributor.affiliatedHyman, Bradley


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