Karen J Miller1, Steven A Rogers, Prabha Siddarth, Gary W Small. 1. Department of Psychiatry and Biobehavioral Sciences, the Neuropsychiatric Institute, the Alzheimer's Disease Center, and the Center on Aging, University of California at Los Angeles, Los Angeles 90024-1759, USA. kmiller@mednet.ucla.edu
Abstract
OBJECTIVES: This study longitudinally examined the object naming and semantic fluency of individuals who are at risk for developing Alzheimer's disease (AD) by virtue of having APOE-4 or a family history of AD. METHODS: A total of 108 participants (40 with a family history of AD and 43 with APOE-4) completed the Boston Naming Test and the Animal Naming task at initial assessment and after two years. RESULTS: At baseline, object naming was significantly lower for those with both risk factors, F(2, 99) = 5.72, p < 0.01, but those with either risk factor had significantly lower scores at follow-up, F(2, 99) = 3.41, p < 0.05. Semantic fluency (animal naming) was reduced among subjects with the APOE-4 allele at baseline, F(1, 100) = 4.02, p < 0.05, but it was not associated with either risk factor at follow-up. CONCLUSIONS: These deficits may be associated with a prodromal risk for AD and may serve as pre-symptomatic markers for the development of AD. 2005 John Wiley & Sons, Ltd.
OBJECTIVES: This study longitudinally examined the object naming and semantic fluency of individuals who are at risk for developing Alzheimer's disease (AD) by virtue of having APOE-4 or a family history of AD. METHODS: A total of 108 participants (40 with a family history of AD and 43 with APOE-4) completed the Boston Naming Test and the Animal Naming task at initial assessment and after two years. RESULTS: At baseline, object naming was significantly lower for those with both risk factors, F(2, 99) = 5.72, p < 0.01, but those with either risk factor had significantly lower scores at follow-up, F(2, 99) = 3.41, p < 0.05. Semantic fluency (animal naming) was reduced among subjects with the APOE-4 allele at baseline, F(1, 100) = 4.02, p < 0.05, but it was not associated with either risk factor at follow-up. CONCLUSIONS: These deficits may be associated with a prodromal risk for AD and may serve as pre-symptomatic markers for the development of AD. 2005 John Wiley & Sons, Ltd.
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