Volume 11, Issue 7S_Part_4 p. P194-P194
Podium Presentations: Monday, July 20, 2015
Free Access

O2-09-01: Impact of ApoE-ɛ4 and family history of dementia on gray matter atrophy in cognitively healthy middle-aged adults

Mara ten Kate

Corresponding Author

Mara ten Kate

VU University Medical Center, Amsterdam, Netherlands

Contact e-mail: [email protected]

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Ernesto Sanz-Arigita

Ernesto Sanz-Arigita

CITA Alzheimer Foundation, San Sebastian, Spain

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Betty M. Tijms

Betty M. Tijms

VU University Medical Center, Amsterdam, Netherlands

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Alle Meije Wink

Alle Meije Wink

VU University Medical Center, Amsterdam, Netherlands

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Montserrat Clerigue

Montserrat Clerigue

CITA Alzheimer Foundation, San Sebastian, Spain

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Maite Garcia-Sebastian

Maite Garcia-Sebastian

CITA Alzheimer Foundation, San Sebastian, Spain

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Andrea Izagirre

Andrea Izagirre

CITA Alzheimer Foundation, San Sebastian, Spain

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Mirian Ecay

Mirian Ecay

CITA Alzheimer Foundation, San Sebastian, Spain

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Ainara Estanga

Ainara Estanga

CITA Alzheimer Foundation, San Sebastian, Spain

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Jorge A. Villanua

Jorge A. Villanua

CITA Alzheimer Foundation, San Sebastian, Spain

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Hugo Vrenken

Hugo Vrenken

VU University Medical Center, Amsterdam, Netherlands

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Pieter Jelle Visser

Pieter Jelle Visser

VU University Medical Center, Amsterdam, Netherlands

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Pablo Martinez-Lage

Pablo Martinez-Lage

CITA Alzheimer Foundation, San Sebastian, Spain

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Frederik Barkhof

Frederik Barkhof

VU University Medical Center, Amsterdam, Netherlands

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First published: 01 July 2015

Background

The apolipoprotein E ε4 allele (APOE4) and family history of dementia (FH) are risk factors for the development of Alzheimer disease (AD). We assessed the effects of both APOE4 and FH on gray matter (GM) density in non-demented middle-aged adults in order to detect brain changes associated with increased risk for AD.

Methods

295 cognitively healthy middle-aged community-dwelling subjects underwent MRI scanning, APOE genotyping and assessment of FH. Voxel-based morphometry was used to study GM density differences between high- and low-risk subjects, based on APOE4 carriership (n=74), first-degree FH (n=227) or both (n=62). Structural brain images were processed and analyzed using VBM8 in SPM8. For statistical analysis, we used a cluster-forming threshold of p < 0.001 uncorrected with a minimal cluster size of 100 voxels.

Results

APOE4 and FH were associated with reduced GM in different brain regions. APOE4 carriers had reduced GM in the striatum compared to non-carriers. Subjects with FH had reduced GM in right precuneus compared to subjects without FH. Maternal and paternal FH provided similar atrophy patterns. APOE4 carriers with FH had GM reductions in bilateral insula compared to subjects with no APOE4 and no FH (figure 1).

Conclusions

FH and APOE4 are both associated with regional GM decreases in cognitively healthy middle-aged subjects, with differential and additive effects on brain regions typically affected in AD.