Age and ApoE genotype interaction in Alzheimer's disease: an FDG-PET study

被引:38
作者
Mosconi, L
Sorbi, S
Nacmias, B
De Cristofaro, MTR
Fayyaz, M
Bracco, L
Herholz, K
Pupi, A
机构
[1] Univ Florence, Nucl Med Unit, Dept Clin Pathophysiol, I-50134 Florence, Italy
[2] Univ Florence, Dept Neurol & Psychiat Sci, Florence, Italy
[3] Univ Cologne, Neurol Clin, Cologne, Germany
[4] Univ Cologne, Max Planck Inst Neurol Res, Cologne, Germany
关键词
positron emission tomography (PET); apolipoprotein E (ApoE); Alzheimer's disease (AD); age; brain metabolism; fluorodeoxyglucose;
D O I
10.1016/j.pscychresns.2003.12.005
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Previous positron emission tomography (PET) studies with fluorodeoxglucose (FDG) as tracer in healthy elders showed that the epsilon4 allele of the apolipoprotein E (ApoE) gene is disruptive to cerebral glucose metabolism (rCMRglu), possibly through the interaction with the aging process. The present study was aimed at assessing whether this interaction occurs in patients with Alzheimer's disease (AD). Eight-six AD patients, including 40 ApoE4 carriers and 46 non-carriers, underwent F-18-FDG PET scanning at rest. ApoE groups were comparable for age, gender, age at onset and disease duration. SPM'99 was used to assess rCMRGlu correlations with age, differences between ApoE groups and ApoE by age interaction, correcting for disease severity. Results were reported at P < 0.001, uncorrected. Correlations between age and rCMRGlu confirmed the well-known negative relationship for both groups. Lower rCMRGlu was found within the frontal and cingulate areas for ApoE4 carriers as compared with the non-carriers. Additionally, a significant ApoE by age interaction was detected in the frontal and anterior cingulate cortex, with the ApoE4 carriers having a steeper regression slope with respect to the non-carriers. These results indicate that age-related regional rCMRglu decreases within the frontal and anterior cingulate areas may be more severe in AD patients carrying the ApoE4 allele. (C) 2003 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:141 / 151
页数:11
相关论文
共 45 条
[1]   THE FLUORODEOXYGLUCOSE F-18 SCAN IN ALZHEIMERS-DISEASE AND MULTI-INFARCT DEMENTIA [J].
BENSON, DF ;
KUHL, DE ;
HAWKINS, RA ;
PHELPS, ME ;
CUMMINGS, JL ;
TSAI, SY .
ARCHIVES OF NEUROLOGY, 1983, 40 (12) :711-714
[2]   Clinicopathologic studies in cognitively healthy aging and Alzheimer disease - Relation of histologic markers to dementia severity, age, sex, and apolipoprotein E genotype [J].
Berg, L ;
McKeel, DW ;
Miller, JP ;
Storandt, M ;
Rubin, EH ;
Morris, JC ;
Baty, J ;
Coats, M ;
Norton, J ;
Goate, AM ;
Price, JL ;
Gearing, M ;
Mirra, SS ;
Saunders, AM .
ARCHIVES OF NEUROLOGY, 1998, 55 (03) :326-335
[3]  
Blass JP, 2000, ANN NY ACAD SCI, V924, P170
[4]   Cerebral blood flow in depressed patients: a methodological comparison of statistical parametric mapping and region of interest analyses [J].
Bonne, O ;
Louzoun, Y ;
Aharon, I ;
Krausz, Y ;
Karger, H ;
Lerer, B ;
Bocher, M ;
Freedman, N ;
Chisin, R .
PSYCHIATRY RESEARCH-NEUROIMAGING, 2003, 122 (01) :49-57
[5]   STAGING OF ALZHEIMERS-DISEASE-RELATED NEUROFIBRILLARY CHANGES [J].
BRAAK, H ;
BRAAK, E .
NEUROBIOLOGY OF AGING, 1995, 16 (03) :271-278
[6]  
Buttini M, 2002, J NEUROSCI, V22, P10539
[7]   No difference in cerebral glucose metabolism in patients with Alzheimer disease and differing apolipoprotein E genotypes [J].
Corder, EH ;
Jelic, V ;
Basun, H ;
Lannfelt, L ;
Valind, S ;
Winblad, B ;
Nordberg, A .
ARCHIVES OF NEUROLOGY, 1997, 54 (03) :273-277
[8]   PROTECTIVE EFFECT OF APOLIPOPROTEIN-E TYPE-2 ALLELE FOR LATE-ONSET ALZHEIMER-DISEASE [J].
CORDER, EH ;
SAUNDERS, AM ;
RISCH, NJ ;
STRITTMATTER, WJ ;
SCHMECHEL, DE ;
GASKELL, PC ;
RIMMLER, JB ;
LOCKE, PA ;
CONNEALLY, PM ;
SCHMADER, KE ;
SMALL, GW ;
ROSES, AD ;
HAINES, JL ;
PERICAKVANCE, MA .
NATURE GENETICS, 1994, 7 (02) :180-184
[9]   GENE DOSE OF APOLIPOPROTEIN-E TYPE-4 ALLELE AND THE RISK OF ALZHEIMERS-DISEASE IN LATE-ONSET FAMILIES [J].
CORDER, EH ;
SAUNDERS, AM ;
STRITTMATTER, WJ ;
SCHMECHEL, DE ;
GASKELL, PC ;
SMALL, GW ;
ROSES, AD ;
HAINES, JL ;
PERICAKVANCE, MA .
SCIENCE, 1993, 261 (5123) :921-923
[10]   CLINICAL HISTORY, BRAIN METABOLISM, AND NEUROPSYCHOLOGICAL FUNCTION IN ALZHEIMERS-DISEASE [J].
CUTLER, NR ;
HAXBY, JV ;
DUARA, R ;
GRADY, CL ;
KAY, AD ;
KESSLER, RM ;
SUNDARAM, M ;
RAPOPORT, SI .
ANNALS OF NEUROLOGY, 1985, 18 (03) :298-309