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Aβ amyloid, cognition, and APOE genotype in healthy older adults
Author(s) -
Lim Yen Ying,
Ellis Kathryn A.,
Ames David,
Darby David,
Harrington Karra,
Martins Ralph N.,
Masters Colin L.,
Rowe Christopher,
Savage Greg,
Szoeke Cassandra,
Villemagne Victor L.,
Maruff Paul
Publication year - 2013
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2012.07.004
Subject(s) - apolipoprotein e , episodic memory , cognition , psychology , effects of sleep deprivation on cognitive performance , audiology , association (psychology) , visual memory , neuroscience , medicine , disease , psychotherapist
Background Only one study has investigated the relationship between cerebral β‐amyloid (Aβ), apolipoprotein E ( APOE ) ɛ4 genotype, and cognition. Although significant relationships between cerebral Aβ and cognition were observed in ɛ4 carriers but not noncarriers, the magnitude of this relationship was not reported. Further, when demographic variables were controlled, the influence of APOE ɛ4 on the relationship between cerebral Aβ and cognition dissipated. Methods In 144 healthy older adults who had undergone amyloid scanning and APOE ɛ4 genotyping in the Australian Imaging, Biomarkers, and Lifestyle (AIBL) Flagship Study of Ageing, correlations were conducted to determine the magnitude of relationship between cerebral Aβ and cognition in ɛ4 carriers and noncarriers. Fisher's Z was used to compare these correlations and Cohen's q determined the magnitude of difference between correlations. Results Cerebral Aβ was significantly associated with tasks of visual and verbal episodic memory in APOE ɛ4 carriers. This association was not observed in ɛ4 noncarriers. The relationship between cerebral Aβ and episodic memory in ɛ4 carriers was significantly different from that in ɛ4 noncarriers, and the magnitude of this difference was small to moderate. Conclusions In APOE ɛ4 carriers, there is a moderate negative relationship between cerebral Aβ and episodic memory. This suggests that increased cerebral Aβ may signify the onset of preclinical AD, especially in healthy older adults who are genetically at risk for AD.