High cerebral amyloid-beta load is linked to a greater decline in episodic and working memory in healthy, cognitively normal adults during an 18-month period than is APOE ε4 genotype, according to research published in the October 16 Neurology. The APOE ε4 genotype was associated with a decline in visual memory, but the effect was less than that observed for cerebral amyloid-beta load.
To evaluate the significance of elevated cerebral amyloid-beta load in relation to long-term cognitive changes, Yen Ying Lim, MPsych, of the University of Melbourne in Victoria, Australia, and colleagues prospectively studied 141 healthy and cognitively normal older adults with a mean age of 76. At baseline and at 18 months, participants completed medical, psychiatric, and neuropsychologic assessments as part of their enrollment in the Australian Imaging Biomarkers and Lifestyle flagship study of aging. In addition to APOE ε4 genotyping, participants underwent Pittsburgh compound B PET imaging that resulted in a region/cerebellar ratio called the standardized uptake value ratio. Subjects also completed a battery of neuropsychologic tests to measure working memory and verbal and visual episodic memory.
Linear mixed-model analyses adjusted for baseline cognitive function showed that persons with high cerebral amyloid-beta load had significantly greater decline on all measures of working memory and verbal and visual episodic memory at 18 months, compared with persons with low cerebral amyloid-beta load. Furthermore, those who carried the APOE ε4 allele had a greater decline in visual memory after 18 months compared with noncarriers. There was no interaction between APOE ε4 allele and cerebral amyloid-beta load for any cognitive measure, the investigators said.