Investigating the influence of KIBRA and CLSTN2 genetic polymorphisms on cross-sectional and longitudinal measures of memory performance and hippocampal volume in older individuals

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

  • Boraxbekk, Carl-Johan Oskar
  • David Ames
  • Nicole A. Kochan
  • Teresa Lee
  • Anbupalam Thalamuthu
  • Wei Wen
  • Nicola J. Armstrong
  • John B.J. Kwok
  • Schofield, Peter
  • Simone Reppermund
  • Margaret J. Wright
  • Julian N. Trollor
  • Henry Brodaty
  • Perminder Sachdev
  • Karen A. Mather

The variability of episodic memory decline and hippocampal atrophy observed with increasing age may partly be explained by genetic factors. KIBRA (kidney and brain expressed protein) and CLSTN2 (calsyntenin 2) are two candidate genes previously linked to episodic memory performance and volume of the hippocampus, a key memory structure. However, whether polymorphisms in these two genes also influence age-related longitudinal memory decline and hippocampal atrophy is still unknown. Using data from two independent cohorts, the Sydney Memory and Ageing Study and the Older Australian Twins Study, we investigated whether the KIBRA and CLSTN2 genetic polymorphisms (rs17070145 and rs6439886) are associated with episodic memory performance and hippocampal volume in older adults (65-90 years at baseline). We were able to examine these polymorphisms in relation to memory and hippocampal volume using cross-sectional data and, more importantly, also using longitudinal data (2 years between testing occasions). Overall we did not find support for an association of KIBRA either alone or in combination with CLSTN2 with memory performance or hippocampal volume, nor did variation in these genes influence longitudinal memory decline or hippocampal atrophy in two cohorts of older adults.

OriginalsprogEngelsk
TidsskriftNeuropsychologia
Vol/bind78
Sider (fra-til)10-17
Antal sider8
ISSN0028-3932
DOI
StatusUdgivet - 2015

Bibliografisk note

Funding Information:
We would like to acknowledge and thank the Sydney MAS and OATS participants, their supporters and the respective research teams. The studies are supported by a National and Health Medical Research Council (NHMRC) / Australian Research Council (ARC) Strategic Award 401162 and the NHMRC Program Grants 350833 and 568969 . OATS was facilitated by access to the Australian Twin Registry, which is funded by the NHMRC Enabling Grant 310667 . DNA was extracted by Genetic Repositories Australia, an Enabling Facility supported by the NHMRC Grant 401184 . The genotyping of OATS was partly funded by a Commonwealth Scientific and Industrial Research Organisation Flagship Collaboration Fund Grant. The Australian Government funded Dementia Collaborative Research Centre at the University of New South Wales supports Henry Brodaty. Nicola Armstrong is supported by the NHMRC Project Grant 525453 . Karen Mather is supported by an Alzheimer's Australia Dementia Research Foundation Postdoctoral Fellowship. Both Karen Mather and Simone Reppermund are supported by the NHMRC Capacity Building Grant 568940 . Nicole Kochan is supported by an NHMRC Health Professional Research Fellowship ( RG123148 )

Publisher Copyright:
© 2015 Elsevier Ltd.

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