Complement Receptor type 1 Polymorphisms Associated with Reduced Cortical Volume and Thickness in Healthy Middle-Aged Adults
Mentor 1
Dr. Ira Driscoll
Location
Union Wisconsin Room
Start Date
28-4-2017 1:30 PM
End Date
28-4-2017 4:00 PM
Description
Complement Receptor type 1 (CR1) has been proposed to contribute to the neuropathology of Alzheimer's disease (AD) through the modulation of neurotoxic amyloid-beta plaque metabolism (Rogers et al., 2006). The purpose of the present investigation was to characterize the relationship between CR1 polymorphism (rs1408077) and structural brain integrity (volume and cortical thickness) in healthy middle-aged adults, allowing us to study structural differences that are present years before cognitive impairments attributed to pathological aging may begin. Participants (N = 150; age 40 - 60) underwent genetic testing and magnetic resonance imaging (MRI). Regional brain volumes and cortical thickness were calculated using Freesurfer. Consistent with its role as an AD risk allele (Biffi et al., 2010; Kok et al., 2011), we found that the CR1 rs1408077 T-allele carriers had lower cortical thickness in the bilateral lateral orbitofrontal cortex, right inferior parietal cortex, and right precuneus (p's .05, familywise error corrected). T-allele carriers also had smaller volumes of the precuneus bilaterally and lateral occipital cortices, as well as the right inferior parietal cortex (p's .05). Atrophy of the aforementioned structures has been found to be associated with cognitive impairment as well as mild AD (McDonald et al., 2009). Collectively, these results suggest that the CR1 polymorphisms are related to structural brain differences evident well prior to any overt impairment, making CR1 gene a potential biomarker of AD.
Complement Receptor type 1 Polymorphisms Associated with Reduced Cortical Volume and Thickness in Healthy Middle-Aged Adults
Union Wisconsin Room
Complement Receptor type 1 (CR1) has been proposed to contribute to the neuropathology of Alzheimer's disease (AD) through the modulation of neurotoxic amyloid-beta plaque metabolism (Rogers et al., 2006). The purpose of the present investigation was to characterize the relationship between CR1 polymorphism (rs1408077) and structural brain integrity (volume and cortical thickness) in healthy middle-aged adults, allowing us to study structural differences that are present years before cognitive impairments attributed to pathological aging may begin. Participants (N = 150; age 40 - 60) underwent genetic testing and magnetic resonance imaging (MRI). Regional brain volumes and cortical thickness were calculated using Freesurfer. Consistent with its role as an AD risk allele (Biffi et al., 2010; Kok et al., 2011), we found that the CR1 rs1408077 T-allele carriers had lower cortical thickness in the bilateral lateral orbitofrontal cortex, right inferior parietal cortex, and right precuneus (p's .05, familywise error corrected). T-allele carriers also had smaller volumes of the precuneus bilaterally and lateral occipital cortices, as well as the right inferior parietal cortex (p's .05). Atrophy of the aforementioned structures has been found to be associated with cognitive impairment as well as mild AD (McDonald et al., 2009). Collectively, these results suggest that the CR1 polymorphisms are related to structural brain differences evident well prior to any overt impairment, making CR1 gene a potential biomarker of AD.
