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4 allele on cerebral glucose metabolism in AD is a function of age at onset
From the Departments of Clinical Neurosciences (Drs. Hirono, Hashimoto, Kazui, and Mori), Basic Neurosciences (Dr. Yasuda), and Neuroimaging Research (Drs. Ishii and Sakamoto), Hyogo Institute for Aging Brain and Cognitive Disorders, Himeji, Japan.
Address correspondence and reprint requests to Dr. Nobutsugu Hirono, Clinical Neurosciences, Hyogo Institute for Aging Brain and Cognitive Disorders, 520 Saisho-Ko, Himeji, 670–0981, Japan; e-mail: hirono{at}hiabcd.go.jp
Background: Although the APOE 
4 allele is a well-known risk factor for developing AD, the impact of the 4 allele on clinical manifestations in patients with AD is still controversial. One possible reason for this controversy is that previous studies did not consider the effect of patient age at symptom onset.
Objective: To investigate the possible impact of patient age at onset of AD on the effect of APOE genotype on regional cerebral glucose metabolism (rCMRglc).
Methods: The authors compared rCMRglc between probable AD patients (based on criteria of the National Institute of Neurologic Disease and Stroke/AD and Related Disorders Association) with APOE 4/4 and APOE 3/3 alleles in early-onset (
65 years old) and late-onset (>65 years old) groups. In each group, the patients with APOE 4/4 and APOE 3/3 alleles were comparable for age at onset, age at examination, sex, disease duration, education level, and severity of dementia.
Results: In the early-onset group, the patients with the APOE 4/4 genotype showed a significant decrease of rCMRglc in the medial temporal lobe and a significant increase of rCMRglc in the inferior parietal and posterior temporal cortices as compared with those patients with the APOE 3/3 genotype. In the late-onset group, there were no significant differences in the rCMRglc pattern between the patients with APOE 4/4 and APOE 3/3 alleles.
Conclusions: The current findings indicate that the impact of the APOE 4 genotype on cerebral glucose metabolism of patients with AD may be a function of age at symptom onset.
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