Title

Fluoro-2-Deoxy-D-Glucose (FDG)-PET in APOE epsilon 4 Carriers in the Australian Population

Document Type

Journal Article

Publisher

IOS Press

Faculty

Computing, Health and Science

School

Exercise, Biomedical and Health Science, Centre for Alzheimer's Disease

RAS ID

5820

Comments

This article was originally published as: Rimajova, M. , Lenzo, N. , Wu, J., Bates, K. A., Campbell, A., Dhaliwald, S., McCarthy, M., Rodrigues, M., Paton, A. , Rowe, C., Foster, J. K., & Martins, R. N. (2008). Fluoro-2-deoxy-D-glucose (FDG)-PET in APOE epsilon 4 carriers in the Australian population . Journal of Alzheimer's Disease, 13(2), 137-146. Original article available here

Abstract

Apolipoprotein E-ϵ4 (APOEε4) has been associated with increased risk of developing Alzheimer's disease (AD) and regional cerebral glucose hypometabolism, as measured by fluoro-2-deoxy-D-glucose-positron emission tomography (FDG-PET). We report here preliminary data from studies that aim to determine whether cerebral glucose hypometabolism is observed in APOEε4 positive, cognitively intact individuals between the ages of 50 and 80, and whether there is an additional impact of subjective memory complainer (SMC) status on glucose metabolism determined by NeuroStat analysis. FDG-PET was conducted in 30 community dwelling, APOE-ε4 carriers without clinical evidence of dementia and objective cognitive impairment as assessed using a neuropsychological battery. Neurological soft-signs (NSS) were also assessed. Glucose hypometabolism was demonstrated in the anterior and posterior cingulate cortex and in the temporal association cortices in APOEε4 carriers compared to the normative NeuroStat database. This pattern was particularly evident in APOEε4 heterozygous individuals. SMC showed hypometabolism in the aforementioned brain regions, whereas non-SMC showed no significant pattern of glucose hypometabolism. FDG-PET with NeuroStat analysis showed that APOEε4 carriers have mild glucose hypometabolism in areas associated with AD. SMC may be associated with AD-related differences in regional cerebral glucose metabolism. These findings are currently being investigated in a larger group of APOEε4 carriers.