PMID- 7884953 OWN - NLM STAT- MEDLINE DCOM- 19950412 LR - 20220330 IS - 0098-7484 (Print) IS - 0098-7484 (Linking) VI - 273 IP - 12 DP - 1995 Mar 22-29 TI - Apolipoprotein E type 4 allele and cerebral glucose metabolism in relatives at risk for familial Alzheimer disease. PG - 942-7 AB - 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. FAU - Small, G W AU - Small GW AD - Department of Psychiatry, University of California, Los Angeles School of Medicine. FAU - Mazziotta, J C AU - Mazziotta JC FAU - Collins, M T AU - Collins MT FAU - Baxter, L R AU - Baxter LR FAU - Phelps, M E AU - Phelps ME FAU - Mandelkern, M A AU - Mandelkern MA FAU - Kaplan, A AU - Kaplan A FAU - La Rue, A AU - La Rue A FAU - Adamson, C F AU - Adamson CF FAU - Chang, L AU - Chang L AU - et al. LA - eng GR - U24 AG021886/AG/NIA NIH HHS/United States GR - 1R29 MH46424/MH/NIMH NIH HHS/United States GR - AG05128/AG/NIA NIH HHS/United States GR - AG10123/AG/NIA NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - JAMA JT - JAMA JID - 7501160 RN - 0 (Apolipoprotein E4) RN - 0 (Apolipoproteins E) RN - 0 (Fluorine Radioisotopes) RN - 0Z5B2CJX4D (Fluorodeoxyglucose F18) RN - 9G2MP84A8W (Deoxyglucose) RN - IY9XDZ35W2 (Glucose) SB - IM MH - Adult MH - Aged MH - Aged, 80 and over MH - Alleles MH - Alzheimer Disease/*genetics/*metabolism/physiopathology MH - Analysis of Variance MH - Apolipoprotein E4 MH - *Apolipoproteins E/genetics/physiology MH - Brain/diagnostic imaging/*metabolism/pathology/physiology MH - Deoxyglucose/analogs & derivatives MH - Family MH - Female MH - Fluorine Radioisotopes MH - Fluorodeoxyglucose F18 MH - Genotype MH - Glucose/*metabolism MH - Humans MH - Magnetic Resonance Imaging MH - Male MH - Middle Aged MH - Models, Theoretical MH - Neuropsychological Tests MH - Risk Factors MH - Tomography, Emission-Computed EDAT- 1995/03/22 00:00 MHDA- 1995/03/22 00:01 CRDT- 1995/03/22 00:00 PHST- 1995/03/22 00:00 [pubmed] PHST- 1995/03/22 00:01 [medline] PHST- 1995/03/22 00:00 [entrez] PST - ppublish SO - JAMA. 1995 Mar 22-29;273(12):942-7.