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    Klotho allele status is not associated with Aß and APOE e4–related cognitive decline in preclinical Alzheimer's disease

    Access Status
    Fulltext not available
    Authors
    Porter, T.
    Burnham, S.
    Milicic, L.
    Savage, G.
    Maruff, P.
    Lim, Y.
    Ames, D.
    Masters, C.
    Martins, R.
    Rainey-Smith, S.
    Rowe, C.
    Salvado, O.
    Groth, David
    Verdile, Giuseppe
    Villemagne, V.
    Laws, S.
    Date
    2019
    Type
    Journal Article
    
    Metadata
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    Citation
    Porter, 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.
    Source Title
    Neurobiology of Aging
    DOI
    10.1016/j.neurobiolaging.2018.12.014
    ISSN
    0197-4580
    School
    School of Pharmacy and Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/73742
    Collection
    • Curtin Research Publications
    Abstract

    © 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.

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