Race modifies default mode connectivity in Alzheimer's disease

• Authors: Maria B. Misiura, Georgia State University; J. Christina Howell, Emory University; Junjie Wu, Emory University; Deqiang Qiu, Emory University; Monica Parker, Emory University; Jessica A. Turner, Georgia State University; William Hu, Emory University
• Journal Title: Translational Neurodegeneration
• Volume: Volume 9, Number 1
• Publisher: BMC | 2020-02-19, Pages 8-8
• Type of Work: Article | Final Publisher PDF
• Publisher DOI: http://doi.org/10.1186/s40035-020-0186-4
• Subjects: Biology, Neuroscience
• Keywords: Science & Technology; Life Sciences & Biomedicine; Neurosciences; Neurosciences & Neurology; Alzheimer's disease; Cognitive impairment; Functional connectivity; Default mode network; Disparities; MILD COGNITIVE IMPAIRMENT; FUNCTIONAL CONNECTIVITY; AFRICAN-AMERICANS; BRAIN ACTIVITY; NETWORK; DEMENTIA; STRESS; RISK; MRI; SUBSYSTEMS

Abstract

Background: Older African Americans are more likely to develop Alzheimer's disease (AD) than older Caucasians, and this difference cannot be readily explained by cerebrovascular and socioeconomic factors alone. We previously showed that mild cognitive impairment and AD dementia were associated with attenuated increases in the cerebrospinal fluid (CSF) levels of total and phosphorylated tau in African Americans compared to Caucasians, even though there was no difference in beta-amyloid 1-42 level between the two races. Methods: We extended our work by analyzing early functional magnetic resonance imaging (fMRI) biomarkers of the default mode network in older African Americans and Caucasians. We calculated connectivity between nodes of the regions belonging to the various default mode network subsystems and correlated these imaging biomarkers with non-imaging biomarkers implicated in AD (CSF amyloid, total tau, and cognitive performance). Results: We found that race modifies the relationship between functional connectivity of default mode network subsystems and cognitive performance, tau, and amyloid levels. Conclusion: These findings provide further support that race modifies the AD phenotypes downstream from cerebral amyloid deposition, and identifies key inter-subsystem connections for deep imaging and neuropathologic characterization.