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APOE*E4 Is Associated with Gray Matter Loss in the Posterior Cingulate Cortex in Healthy Elderly Controls Subsequently Developing Subtle Cognitive Decline
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Radiologi. Affidea Ctr Diagnost Radiol Carouge, Geneva, Switzerland.;Univ Geneva, Fac Med, Geneva, Switzerland.;Univ Hosp Freiburg, Dept Neuroradiol, Freiburg, Germany..ORCID-id: 0000-0001-7433-0203
Univ Hosp Geneva, Dept Mental Hlth & Psychiat, Geneva, Switzerland.
Univ Hosp Geneva, Div Inst Measures, Med Direct, Geneva, Switzerland..
Univ Hosp Geneva, Dept Mental Hlth & Psychiat, Geneva, Switzerland..
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2017 (Engelska)Ingår i: American Journal of Neuroradiology, ISSN 0195-6108, E-ISSN 1936-959X, Vol. 38, nr 7, s. 1335-1342Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

BACKGROUND AND PURPOSE: The presence of apolipoprotein E4 (APOE*E4) is the strongest currently known genetic risk factor for Alzheimer disease and is associated with brain gray matter loss, notably in areas involved in Alzheimer disease pathology. Our objective was to assess the effect of APOE*E4 on brain structures in healthy elderly controls who subsequently developed subtle cognitive decline.

MATERIALS AND METHODS: This prospective study included 382 community-dwelling elderly controls. At baseline, participants underwent MR imaging at 3T, extensive neuropsychological testing, and genotyping. After neuropsychological follow-up at 18 months, participants were classified into cognitively stable controls and cognitively deteriorating controls. Data analysis included whole-brain voxel-based morphometry and ROI analysis of GM.

RESULTS: APOE*E4-related GM loss at baseline was found only in the cognitively deteriorating controls in the posterior cingulate cortex. There was no APOE*E4-related effect in the hippocampus, mesial temporal lobe, or brain areas not involved in Alzheimer disease pathology. Controls in the cognitively deteriorating group had slightly lower GM concentration in the hippocampus at baseline. Higher GM densities in the hippocampus, middle temporal lobe, and amygdala were associated with a decreased risk for cognitively deteriorating group status at follow-up.

CONCLUSIONS: APOE*E4-related GM loss in the posterior cingulate cortex (an area involved in Alzheimer disease pathology) was found only in those elderly controls who subsequently developed subtle cognitive decline but not in cognitively stable controls. This finding might explain the partially conflicting results of previous studies that typically did not include detailed neuropsychological assessment and follow-up. Most important, APOE*E4 status had no impact on GM density in areas affected early by neurofibrillary tangle formation such as the hippocampus and mesial temporal lobe.

Ort, förlag, år, upplaga, sidor
2017. Vol. 38, nr 7, s. 1335-1342
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
URN: urn:nbn:se:uu:diva-332199DOI: 10.3174/ajnr.A5184ISI: 000405565100013PubMedID: 28495939OAI: oai:DiVA.org:uu-332199DiVA, id: diva2:1152889
Tillgänglig från: 2017-10-26 Skapad: 2017-10-26 Senast uppdaterad: 2017-10-31Bibliografiskt granskad

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