Event Title

Apolipoprotein E Polymorphisms Associated with Reduced Subcortical Volume and Cortical Thickness in Healthy Middle-Aged Adults

Mentor 1

Dr. Ira Driscoll

Location

Union Wisconsin Room

Start Date

29-4-2016 1:30 PM

End Date

29-4-2016 3:30 PM

Description

The pathology associated with Alzheimer's disease (AD) includes hippocampal atrophy and medial temporal lobe changes. Characterizing genes associated with these physiological differences can offer insight into the etiology of the disease. APOE has been established as the best known genetic risk factor for AD. The purpose of the current study was to characterize the relationships between APOE SNPs (rs429358 and rs157580) and structural brain integrity (brain volume and cortical thickness). We focus on studying brain integrity in middle age, years before the onset of clinical symptoms of AD, as altered structural brain integrity at this age may serve as an early biomarker of age-related cognitive decline. Healthy middle-aged adults (40-60 years) underwent both genetic testing and magnetic resonance imaging (MRI). Regional brain volumes and cortical thickness were calculated using Freesurfer. APOE (rs157580) risk allele carriers (ε4) had significantly lower right entorhinal cortex (p = .04) and a trend toward smaller right parahippocampal cortex (p = .08) volumes compared to non-ε4 carriers. Regarding APOE rs429358, minor allele (G) carriers had smaller volumes of the right (p = .04) and left (p = .01) entorhinal cortices as well as the left parahippocampal cortex (p = .003). There was a trend towards lower volume in the right parahippocampal cortex (p = .08). Minor allele (G) carriers also had thinner cortex in the right inferior temporal gyrus (p = .03) and left superior temporal sulcus (p = .04). While not significant, there was also a trend toward minor allele carriers having thinner cortex in the left lateral superior temporal sulcus (p = .07) and left superior temporal gyrus (p = .05). These results suggest that polymorphism in the APOE gene may contribute to altered structural brain integrity well before the typical age of AD onset, making it a potential biomarker for risk of AD.

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Apr 29th, 1:30 PM Apr 29th, 3:30 PM

Apolipoprotein E Polymorphisms Associated with Reduced Subcortical Volume and Cortical Thickness in Healthy Middle-Aged Adults

Union Wisconsin Room

The pathology associated with Alzheimer's disease (AD) includes hippocampal atrophy and medial temporal lobe changes. Characterizing genes associated with these physiological differences can offer insight into the etiology of the disease. APOE has been established as the best known genetic risk factor for AD. The purpose of the current study was to characterize the relationships between APOE SNPs (rs429358 and rs157580) and structural brain integrity (brain volume and cortical thickness). We focus on studying brain integrity in middle age, years before the onset of clinical symptoms of AD, as altered structural brain integrity at this age may serve as an early biomarker of age-related cognitive decline. Healthy middle-aged adults (40-60 years) underwent both genetic testing and magnetic resonance imaging (MRI). Regional brain volumes and cortical thickness were calculated using Freesurfer. APOE (rs157580) risk allele carriers (ε4) had significantly lower right entorhinal cortex (p = .04) and a trend toward smaller right parahippocampal cortex (p = .08) volumes compared to non-ε4 carriers. Regarding APOE rs429358, minor allele (G) carriers had smaller volumes of the right (p = .04) and left (p = .01) entorhinal cortices as well as the left parahippocampal cortex (p = .003). There was a trend towards lower volume in the right parahippocampal cortex (p = .08). Minor allele (G) carriers also had thinner cortex in the right inferior temporal gyrus (p = .03) and left superior temporal sulcus (p = .04). While not significant, there was also a trend toward minor allele carriers having thinner cortex in the left lateral superior temporal sulcus (p = .07) and left superior temporal gyrus (p = .05). These results suggest that polymorphism in the APOE gene may contribute to altered structural brain integrity well before the typical age of AD onset, making it a potential biomarker for risk of AD.