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Lack Of Association Of Apolipoprotein E ε4 Allele Dose With Cerebral Glucose Metabolism In Alzheimer Disease

N. Hirono, E. Mori, M. Yasuda, K. Ishii, Y. Ikejiri, T. Imamura, T. Shimomura, M. Hashimoto, H. Yamashita, M. Sasaki
Published 1998 · Biology

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Summary:Parietal cerebral glucose metabolism is reduced before substantial impairments appeared in subjects carrying the apolipoprotein E (APOE) ε4 allele, but the effect of the APOE ε4 allele on cerebral metabolism in Alzheimer disease (AD) is still undetermined. To investigate the effect of the APOE ε4 allele on cerebral metabolism in AD, we examined regional cerebral glucose metabolism in 83 patients with AD by using 18F-fluorodeoxyglucose and positron emission tomography. Cerebral glucose metabolism in the fronto-parieto-temporal association and limbic cortices was significantly decreased in the AD patients compared with 26 age- and sex-matched normal controls. Regional cerebral glucose metabolic rate was not correlated significantly with the number of APOE ε4 alleles in any region, which was consistent even after controlling the effects of age, sex, and severity of dementia, and in a subgroup analysis of those aged between 60 and 75. These results supported the view that the APOE ε4 allele is not associated with specific deficits in brain metabolism in AD despite evidence of preclinical alterations.



This paper is referenced by
10.3390/jcm8050651
Vascular Dysfunction in Alzheimer’s Disease: A Prelude to the Pathological Process or a Consequence of It?
Karan Govindpani (2019)
10.1016/j.pscychresns.2013.09.006
APOE associated hemispheric asymmetry of entorhinal cortical thickness in aging and Alzheimer's disease
M. Donix (2013)
10.1111/j.1447-0594.2012.00934.x
Rate of progression of Alzheimer's disease in younger versus older patients: A longitudinal single photon emission computed tomography study
M. Sakai (2013)
10.1002/ima.22004
Positron emission tomography in neurological and psychiatric disorders
A. Newberg (2012)
10.1186/1471-2202-9-S2-S16
Hypometabolism as a therapeutic target in Alzheimer's disease
L. Costantini (2008)
10.1007/BF03033995
Decreased cerebral blood flow and prognosis of Alzheimer's disease: A multicenter HMPAO-SPECT study
T. Nishimura (2007)
10.1159/000109150
Neuroimaging and APOE Genotype: A Systematic Qualitative Review
N. Cherbuin (2007)
10.1212/01.WNL.0000148478.39691.D3
Cerebral glucose metabolism in patients with AD and different APOE genotypes
A. Drzezga (2005)
10.1176/APPI.NEUROPSYCH.16.4.488
One-year change in cerebral glucose metabolism in patients with Alzheimer's disease.
N. Hirono (2004)
10.1016/j.pscychresns.2003.12.005
Age and ApoE genotype interaction in Alzheimer's disease: an FDG-PET study
L. Mosconi (2004)
10.1136/jnnp.2003.014993
Brain metabolic decreases related to the dose of the ApoE e4 allele in Alzheimer’s disease
L. Mosconi (2004)
10.1016/S0079-6123(03)45021-8
Functional studies of cholinergic activity in normal and Alzheimer disease states by imaging technique.
A. Nordberg (2004)
10.1007/978-3-642-59300-0_12
Positron Emission Tomography and Magnetic Resonance Imaging in the Study of Cognitively Normal Persons at Differential Genetic Risk for Alzheimer’s Dementia
E. Reiman (2004)
10.1176/JNP.15.1.78
Influence of the apolipoprotein E type 4 allele on cerebral glucose metabolism in Alzheimer's disease patients.
Kang-Uk Lee (2003)
10.1111/j.1552-6569.2003.tb00167.x
Apolipoprotein E Genotype and Early Alzheimer's Disease: A Longitudinal SPECT Study
Shigeki Sakamoto (2003)
10.1037/0894-4105.17.3.339
Role of white matter lesions, cerebral atrophy, and APOE on cognition in older persons with and without dementia: the Cache County, Utah, study of memory and aging.
E. Bigler (2003)
10.1159/000070851
Cerebral Correlates of the Progression Rate of the Cognitive Decline in Probable Alzheimer’s Disease
Y. Nagahama (2003)
10.1073/pnas.2635903100
Functional brain abnormalities in young adults at genetic risk for late-onset Alzheimer's dementia
E. Reiman (2003)
10.1053/SNUC.2002.29276
Determination of regional cerebral function with FDG-PET imaging in neuropsychiatric disorders.
A. Newberg (2002)
10.1002/ana.10093
Accelerated hippocampal atrophy in Alzheimer's disease with apolipoprotein E ε4 allele
E. Mori (2002)
10.1212/WNL.58.5.743
The effect of APOE &egr;4 allele on cerebral glucose metabolism in AD is a function of age at onset
N. Hirono (2002)
10.1161/01.STR.32.7.1514
Effect of Apolipoprotein E Genotype on Cerebral Autoregulation During Cardiopulmonary Bypass
L. Ti (2001)
10.1007/BF02988596
Cerebral blood flow and metabolic abnormalities in Alzheimer’s disease
H. Matsuda (2001)
10.1177/089198870101400110
Single Photon Emission Computed Tomography and Apolipoprotein E in Alzheimer's Disease: Impact of the ε4 Allele on Regional Cerebral Blood Flow
P. Høgh (2001)
Use of Positron Emission Tomography and Other Neuroimaging Techniques in the Diagnosis and Management of Alzheimer’s Disease and Dementia
D. Matchar (2001)
10.1212/WNL.57.8.1461
Apolipoprotein E ε4 and the pattern of regional brain atrophy in Alzheimer’s disease
M. Hashimoto (2001)
10.1016/S0197-4580(00)00120-2
How does the apolipoprotein E genotype modulate the brain in aging and in Alzheimer’s disease? A review of neuroimaging studies
M. Lehtovirta (2000)
10.1159/000017227
Features of Regional Cerebral Glucose Metabolism Abnormality in Corticobasal Degeneration
N. Hirono (2000)
10.1002/(SICI)1099-1077(200001)15:1<1::AID-HUP153>3.0.CO;2-1
A unifying hypothesis of Alzheimer's disease. III. Risk factors
K. Heininger, (2000)
10.1073/PNAS.090106797
Cerebral metabolic and cognitive decline in persons at genetic risk for Alzheimer's disease.
G. Small (2000)
10.1097/00002093-200000001-00016
Early Diagnosis of Alzheimer Disease With Positron Emission Tomography
V. Jelic (2000)
10.1002/1531-8249(200009)48:3<297::AID-ANA3>3.0.CO;2-Z
Mitochondrial damage in Alzheimer's disease varies with apolipoprotein E genotype
G. Gibson (2000)
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