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dc.date.accessioned2016-02-08T09:44:11Z
dc.date.available2016-02-08T09:44:11Z
dc.date.created2014-03-28T15:02:16Z
dc.date.issued2015
dc.identifier.citationFjell, Anders Martin Amlien, Inge Sneve, Markus Handal Grydeland, Håkon Tamnes, Christian Krog Chaplin, Tristan Rosa, Marcello Walhovd, Kristine B . The Roots of Alzheimer’s Disease: Are High-Expanding Cortical Areas Preferentially Targeted?. Cerebral Cortex. 2015, 2556-2565
dc.identifier.urihttp://hdl.handle.net/10852/48985
dc.description.abstractAlzheimer's disease (AD) is regarded a human-specific condition, and it has been suggested that brain regions highly expanded in humans compared with other primates are selectively targeted. We calculated shared and unique variance in the distribution of AD atrophy accounted for by cortical expansion between macaque and human, affiliation to the default mode network (DMN), ontogenetic development and normal aging. Cortical expansion was moderately related to atrophy, but a critical discrepancy was seen in the medial temporo-parietal episodic memory network. Identification of “hotspots” and “coldspots” of expansion across several primate species did not yield compelling evidence for the hypothesis that highly expanded regions are specifically targeted. Controlling for distribution of atrophy in aging substantially attenuated the expansion–AD relationship. A path model showed that all variables explained unique variance in AD atrophy but were generally mediated through aging. This supports a systems-vulnerability model, where critical networks are subject to various negative impacts, aging in particular, rather than being selectively targeted in AD. An alternative approach is suggested, focused on the interplay of the phylogenetically old and preserved medial temporal lobe areas with more highly expanded association cortices governed by different principles of plasticity and stability. This is a pre-copyedited, author-produced PDF of an article accepted for publication in Cerebral Cortex following peer review. The version of record is available online at: http://dx.doi.org/10.1093/cercor/bhu055en_US
dc.languageEN
dc.language.isoenen_US
dc.publisherOxford University Press
dc.titleThe Roots of Alzheimer’s Disease: Are High-Expanding Cortical Areas Preferentially Targeted?en_US
dc.typeJournal articleen_US
dc.creator.authorFjell, Anders Martin
dc.creator.authorAmlien, Inge
dc.creator.authorSneve, Markus Handal
dc.creator.authorGrydeland, Håkon
dc.creator.authorTamnes, Christian Krog
dc.creator.authorChaplin, Tristan
dc.creator.authorRosa, Marcello
dc.creator.authorWalhovd, Kristine B
cristin.unitcode185,17,5,0
cristin.unitnamePsykologisk institutt
cristin.ispublishedtrue
cristin.fulltextpostprint
cristin.qualitycode2
dc.identifier.cristin1125660
dc.identifier.bibliographiccitationinfo:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Cerebral Cortex&rft.volume=&rft.spage=2556&rft.date=2015
dc.identifier.jtitleCerebral Cortex
dc.identifier.volume25
dc.identifier.issue9
dc.identifier.startpage2556
dc.identifier.endpage2565
dc.identifier.doihttp://dx.doi.org/10.1093/cercor/bhu055
dc.identifier.urnURN:NBN:no-52805
dc.type.documentTidsskriftartikkelen_US
dc.type.peerreviewedPeer reviewed
dc.source.issn1047-3211
dc.identifier.fulltextFulltext https://www.duo.uio.no/bitstream/handle/10852/48985/1/Fjell%2Bet%2Bal%2BCerCor%2BAD%2Bevolution.pdf
dc.type.versionAcceptedVersion


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