Dataset Information

Association of plasma and cortical amyloid beta is modulated by APOE ?4 status.

ABSTRACT: BACKGROUND:Apolipoprotein E (APOE) ?4 allele's role as a modulator of the relationship between soluble plasma amyloid beta (A?) and fibrillar brain A? measured by Pittsburgh compound B positron emission tomography ([(11)C]PiB PET) has not been assessed. METHODS:Ninety-six Alzheimer's Disease Neuroimaging Initiative participants with [(11)C]PiB scans and plasma A?1-40 and A?1-42 measurements at the time of PET scanning were included. Regional and voxelwise analyses of [(11)C]PiB data were used to determine the influence of APOE ?4 allele on association of plasma A?1-40, A?1-42, and A?1-40/A?1-42 with [(11)C]PiB uptake. RESULTS:In APOE ?4- but not ?4+ participants, positive relationships between plasma A?1-40/A?1-42 and [(11)C]PiB uptake were observed. Modeling the interaction of APOE and plasma A?1-40/A?1-42 improved the explained variance in [(11)C]PiB binding compared with using APOE and plasma A?1-40/A?1-42 as separate terms. CONCLUSIONS:The results suggest that plasma A? is a potential Alzheimer's disease biomarker and highlight the importance of genetic variation in interpretation of plasma A? levels.

SUBMITTER: Swaminathan S

PROVIDER: S-EPMC3750076 | biostudies-literature | 2014 Jan

REPOSITORIES: biostudies-literature

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Association of plasma and cortical amyloid beta is modulated by APOE ε4 status.

Swaminathan Shanker S Risacher Shannon L SL Yoder Karmen K KK West John D JD Shen Li L Kim Sungeun S Inlow Mark M Foroud Tatiana T Jagust William J WJ Koeppe Robert A RA Mathis Chester A CA Shaw Leslie M LM Trojanowski John Q JQ Soares Holly H Aisen Paul S PS Petersen Ronald C RC Weiner Michael W MW Saykin Andrew J AJ

Alzheimer's & dementia : the journal of the Alzheimer's Association 20130326 1

<h4>Background</h4>Apolipoprotein E (APOE) ε4 allele's role as a modulator of the relationship between soluble plasma amyloid beta (Aβ) and fibrillar brain Aβ measured by Pittsburgh compound B positron emission tomography ([(11)C]PiB PET) has not been assessed.<h4>Methods</h4>Ninety-six Alzheimer's Disease Neuroimaging Initiative participants with [(11)C]PiB scans and plasma Aβ1-40 and Aβ1-42 measurements at the time of PET scanning were included. Regional and voxelwise analyses of [(11)C]PiB da ...[more]

PMID: 23541187

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Project description:BackgroundSubjective cognitive decline (SCD) is characterized by self-reported cognitive deficits without measurable cognitive impairment. It has been suggested that individuals with SCD exhibited brain structural alterations in widespread cortical thinning or gray matter loss in the medial temporal and frontotemporal regions. Apolipoprotein E (APOE) ε4 allele is thought to be a genetic marker associated with risk of SCD. Neuropsychiatric symptoms may provide insight in detecting higher-risk elders for early Alzheimer's disease as well. Therefore, we aim to explore the characteristics of brain morphology in SCD and to determine whether it is influenced by APOE ε4 as well as neuropsychiatric symptoms in SCD.MethodsA total of 138 cognitively normal older individuals from the SILCODE cohort underwent a clinical interview, neuropsychological assessments, a blood test, and MRI. A two-sample t-test was used to examine the cortex volume and bilateral cortical surface area alterations between SCD (n = 65) and controls (n = 73). A general linear model analysis was used to test for both main and interaction effects of clinical phenotype (SCD vs. controls) and APOE on global and regional cortex volume and bilateral cortical surface area and thickness. A multiple linear regression analysis was conducted to determine the effects of the APOE genotype on the relationships between morphometric features and neuropsychiatric symptoms in SCD.ResultsCompared with controls, individuals with SCD showed decreased total cortical volumes and cortical surface area. SCD APOE ε4 carriers showed additive reduction in the right cortical surface area. The evaluation scores of anxiety symptoms were negatively associated with the right cortical surface area in SCD APOE 4 non-carriers.ConclusionsIndividuals with SCD had an altered cortical surface area, and APOE genotype and anxiety symptoms are modified factors on the cortical surface area decrease in SCD.Trial registrationClinicalTrials.gov (Identifier: NCT03370744 ). Registered 15 March 2017.

Dataset Information

Association of plasma and cortical amyloid beta is modulated by APOE ?4 status.

Publications

Association of plasma and cortical amyloid beta is modulated by APOE ε4 status.

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