Michelle M Mielke1, Mary M Machulda2, Clinton E Hagen3, Teresa J Christianson3, Rosebud O Roberts4, David S Knopman5, Prashanthi Vemuri6, Val J Lowe6, Walter K Kremers3, Clifford R Jack6, Ronald C Petersen4. 1. Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA; Department of Neurology, Mayo Clinic, Rochester, MN, USA. Electronic address: mielke.michelle@mayo.edu. 2. Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN, USA. 3. Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA. 4. Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA; Department of Neurology, Mayo Clinic, Rochester, MN, USA. 5. Department of Neurology, Mayo Clinic, Rochester, MN, USA. 6. Department of Radiology, Mayo Clinic, Rochester, MN, USA.
Abstract
INTRODUCTION: Few studies have examined the effects of amyloid and apolipoprotein E (APOE) genotype on cognition among middle-aged individuals. METHODS: We included 464 cognitively normal, test-naïve, participants with Pittsburgh compound B positron emission tomography amyloid imaging, mean age of 62.7 (range, 51-71 years), enrolled in the Mayo Clinic Study of Aging. Participants completed multiple cognitive assessments, including a standard neuropsychological battery and the CogState computerized battery, over 30 months of follow-up. Linear mixed models were used to examine the effects of amyloid and APOE genotype on baseline cognition and cognitive decline. RESULTS: Elevated amyloid was not associated with tests of episodic memory but did predict declines on tests of executive function. APOE genotype was not associated with cognition. Among APOE ɛ4 noncarriers, higher amyloid was predictive of decline on tests of executive function and on one episodic memory test. DISCUSSION: Elevated amyloidosis and APOE genotype do not appear to exert a dramatic influence on cognition in middle age.
INTRODUCTION: Few studies have examined the effects of amyloid and apolipoprotein E (APOE) genotype on cognition among middle-aged individuals. METHODS: We included 464 cognitively normal, test-naïve, participants with Pittsburgh compound B positron emission tomography amyloid imaging, mean age of 62.7 (range, 51-71 years), enrolled in the Mayo Clinic Study of Aging. Participants completed multiple cognitive assessments, including a standard neuropsychological battery and the CogState computerized battery, over 30 months of follow-up. Linear mixed models were used to examine the effects of amyloid and APOE genotype on baseline cognition and cognitive decline. RESULTS: Elevated amyloid was not associated with tests of episodic memory but did predict declines on tests of executive function. APOE genotype was not associated with cognition. Among APOE ɛ4 noncarriers, higher amyloid was predictive of decline on tests of executive function and on one episodic memory test. DISCUSSION: Elevated amyloidosis and APOE genotype do not appear to exert a dramatic influence on cognition in middle age.
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