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dc.contributor.authorPorter, T.
dc.contributor.authorBurnham, S.
dc.contributor.authorMilicic, L.
dc.contributor.authorSavage, G.
dc.contributor.authorMaruff, P.
dc.contributor.authorLim, Y.
dc.contributor.authorAmes, D.
dc.contributor.authorMasters, C.
dc.contributor.authorMartins, R.
dc.contributor.authorRainey-Smith, S.
dc.contributor.authorRowe, C.
dc.contributor.authorSalvado, O.
dc.contributor.authorGroth, David
dc.contributor.authorVerdile, Giuseppe
dc.contributor.authorVillemagne, V.
dc.contributor.authorLaws, S.
dc.identifier.citationPorter, T. and Burnham, S. and Milicic, L. and Savage, G. and Maruff, P. and Lim, Y. and Ames, D. et al. 2019. Klotho allele status is not associated with Aß and APOE e4–related cognitive decline in preclinical Alzheimer's disease. Neurobiology of Aging. 76: pp. 162-165.

© 2019 Elsevier Inc. The longevity gene Klotho (KL), specifically the functional KL-VS variant, has previously been associated with cognition and rates of cognitive decline. This study aimed to determine whether KL-VS associations with cognition were observable in preclinical Alzheimer's disease (AD). The study also aimed to determine whether there was a combined influence of KL-VS, neocortical amyloid-ß (Aß) burden, and carriage of the apolipoprotein E (APOE) e4 allele on cognitive decline. This study involved 581 Aß-imaged, cognitively normal older adults, enrolled in the Australian Imaging, Biomarkers and Lifestyle Study of Aging. Linear mixed effects models revealed no significant associations between KL-VS and cognitive decline independently or in combination with Aß burden and APOE e4 genotype. Overall, previous associations reported between KL-VS and cognitive decline are not observed at the preclinical stages of AD. Furthermore, the results do not support the hypothesis that KL-VS has a modifying effect on Aß burden and APOE e4–driven cognitive decline in preclinical AD.

dc.publisherElsevier Inc.
dc.titleKlotho allele status is not associated with Aß and APOE e4–related cognitive decline in preclinical Alzheimer's disease
dc.typeJournal Article
dcterms.source.titleNeurobiology of Aging
curtin.departmentSchool of Pharmacy and Biomedical Sciences
curtin.accessStatusFulltext not available

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