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Apolipoprotein E type 4 allele and cerebral glucose metabolism in
relatives at risk for familial Alzheimer disease
Source: JAMA 1995 Mar;273(12):942-947.
Author: Small GW;Mazziotta JC;Collins MT;Baxter LR;Phelps ME;Mandelkern MA;Kaplan A;La Rue A;Adamson CF;Chang L
PubMed ID: 7884953
Abstract:
OBJECTIVE--Cerebral parietal hypometabolism and left-right asymmetry occur early in the course of Alzheimer disease (AD), and the apolipoprotein E type 4 allele (APOE epsilon 4) is a risk factor for familial AD. To determine if APOE epsilon 4 is associated with lowered brain function in nondemented relatives at risk for familial AD, we studied 12 relatives with APOE epsilon 4 and 19 relatives without APOE epsilon 4. We also compared them with seven patients with probable AD. DESIGN--After grouping subjects according to diagnosis and genotype, brain function measures were compared among groups. SETTING--University medical center. PATIENTS--At risk subjects had mild memory complaints, normal cognitive performance, and at least two relatives with AD. Subjects with APOE epsilon 4 did not differ from those without APOE epsilon 4 in mean age at examination (56.4 vs 55.5 years) or in neuropsychological performance (mean Mini-Mental State Examination score, 28.8 vs 29.3). MAIN OUTCOME MEASURES--Cerebral glucose metabolism was measured using positron emission tomography and fludeoxyglucose F 18. RESULTS--Parietal metabolism was significantly lower and left-right parietal asymmetry was significantly higher in at- risk subjects with APOE epsilon 4 compared with those without APOE epsilon 4. Patients with dementia had significantly lower parietal metabolism than did at-risk subjects with APOE epsilon 4. CONCLUSIONS-- These results suggest that the inheritance of APOE epsilon 4 is associated with reduced cerebral parietal metabolism and increased asymmetry in non-demented relatives at risk for probable AD. Longitudinal study will determine if glucose metabolic measures provide a means to monitor experimental treatment responses during the early phases of the disorder
Source: JAMA 1995 Mar;273(12):942-947.
Author: Small GW;Mazziotta JC;Collins MT;Baxter LR;Phelps ME;Mandelkern MA;Kaplan A;La Rue A;Adamson CF;Chang L
PubMed ID: 7884953
Abstract:
OBJECTIVE--Cerebral parietal hypometabolism and left-right asymmetry occur early in the course of Alzheimer disease (AD), and the apolipoprotein E type 4 allele (APOE epsilon 4) is a risk factor for familial AD. To determine if APOE epsilon 4 is associated with lowered brain function in nondemented relatives at risk for familial AD, we studied 12 relatives with APOE epsilon 4 and 19 relatives without APOE epsilon 4. We also compared them with seven patients with probable AD. DESIGN--After grouping subjects according to diagnosis and genotype, brain function measures were compared among groups. SETTING--University medical center. PATIENTS--At risk subjects had mild memory complaints, normal cognitive performance, and at least two relatives with AD. Subjects with APOE epsilon 4 did not differ from those without APOE epsilon 4 in mean age at examination (56.4 vs 55.5 years) or in neuropsychological performance (mean Mini-Mental State Examination score, 28.8 vs 29.3). MAIN OUTCOME MEASURES--Cerebral glucose metabolism was measured using positron emission tomography and fludeoxyglucose F 18. RESULTS--Parietal metabolism was significantly lower and left-right parietal asymmetry was significantly higher in at- risk subjects with APOE epsilon 4 compared with those without APOE epsilon 4. Patients with dementia had significantly lower parietal metabolism than did at-risk subjects with APOE epsilon 4. CONCLUSIONS-- These results suggest that the inheritance of APOE epsilon 4 is associated with reduced cerebral parietal metabolism and increased asymmetry in non-demented relatives at risk for probable AD. Longitudinal study will determine if glucose metabolic measures provide a means to monitor experimental treatment responses during the early phases of the disorder