Journal article

KIBRA is associated with accelerated cognitive decline and hippocampal atrophy in APOE epsilon 4-positive cognitively normal adults with high A beta-amyloid burden

Tenielle Porter, Samantha C Burnham, Vincent Dore, Greg Savage, Pierrick Bourgeat, Kimberly Begemann, Lidija Milicic, David Ames, Ashley I Bush, Paul Maruff, Colin L Masters, Christopher C Rowe, Stephanie Rainey-Smith, Ralph N Martins, David Groth, Giuseppe Verdile, Victor L Villemagne, Simon M Laws



A single nucleotide polymorphism, rs17070145, in the KIdney and BRAin expressed protein (KIBRA) gene has been associated with cognition and hippocampal volume in cognitively normal (CN) individuals. However, the impact of rs17070145 on longitudinal cognitive decline and hippocampal atrophy in CN adults at greatest risk of developing Alzheimer's disease is unknown. We investigated the impact rs17070145 has on the rate of cognitive decline and hippocampal atrophy over six years in 602 CN adults, with known brain Aβ-amyloid levels and whether there is an interactive effect with APOE genotype. We reveal that whilst limited independent effects of KIBRA genotype were observed, there was an interac..

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Awarded by Cooperative Research Centre (CRC) for Mental Health through CRC Program, an Australian Government Initiative

Funding Acknowledgements

Funding for the AIBL study was provided in part by the study partners [Commonwealth Scientific Industrial and research Organization (CSIRO), Edith Cowan University (ECU), Mental Health Research institute (MHRI), National Ageing Research Institute (NARI), Austin Health, CogState Ltd.]. The AIBL study has also received support from the National Health and Medical Research Council (NHMRC) and the Dementia Collaborative Research Centres program (DCRC2), as well as funding from the Science and Industry Endowment Fund (SIEF) and the Cooperative Research Centre (CRC) for Mental Health - funded through the CRC Program (Grant ID: 20100104), an Australian Government Initiative. We thank all those who took part as subjects in the study for their commitment and dedication to helping advance research into the early detection and causation of AD. We kindly thank all AIBL Research Group members (