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Altered deactivation in individuals with genetic risk for Alzheimer's disease
Stockholms universitet, Samhällsvetenskapliga fakulteten, Psykologiska institutionen.
Vise andre og tillknytning
2008 (engelsk)Inngår i: Neuropsychologia, ISSN 0028-3932, E-ISSN 1873-3514, Vol. 46, nr 6, s. 1679-1687Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Regions that show task-induced deactivations may be part of a default-mode network related to processes that are more engaged during passive than active task conditions. Alteration of task-induced deactivations with age and dementia is indicated by atypical engagement of default-mode network regions. Genetic studies show a relation between the apolipoprotein E4 (<i>APOE4</i>) allele and the common form of Alzheimer’s disease (AD), and altered functional brain activation has been observed in non-demented <i>APOE4</i> carriers compared to non-carriers. Here we investigate the hypothesis of altered default-mode network brain responses in individuals with genetic risk for AD. Functional MRI was used to assess task-induced deactivation in 60 subjects of which 30 carried at least one copy of the <i>APOE4</i> allele, and 30 non-carriers. Subjects were scanned while performing a semantic categorization task shown to promote episodic memory encoding. The results show patterns of deactivation consistent with the default-mode network. We also found reduced deactivation in non-demented <i>APOE4</i> carriers compared to non-carriers, suggesting alterations in the default-mode network in the absence of dementia. These results implicate possibilities for investigatin altered properties of task-induced deactivations in individuals with genetic risk for AD, and may prove useful for pre-clinical identification of individuals susceptible to memory problems and AD.

sted, utgiver, år, opplag, sider
2008. Vol. 46, nr 6, s. 1679-1687
Emneord [en]
deactivation, aging, APOE, genetics, AD, Alzheimer’s disease, fMRI, compensation, memory encoding
HSV kategori
Identifikatorer
URN: urn:nbn:se:su:diva-14738DOI: 10.1016/j.neuropsychologia.2008.01.026ISI: 000257128200010PubMedID: 18346764OAI: oai:DiVA.org:su-14738DiVA, id: diva2:181258
Tilgjengelig fra: 2008-12-04 Laget: 2008-12-04 Sist oppdatert: 2018-11-28bibliografisk kontrollert

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Persson, JonasNilsson, Lars-Göran
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