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Abstract #3002

Sequential PET/MR reveals evidence of parasagittal dural hypertrophy in the setting of elevated Aβ burden in adults with Alzheimer’s disease

Alexander K Song1,2, Kilian Hett1, Jarrod J. Eisma1, Colin D. Mcknight3, Jason Elenberger1, Adam J. Stark1, Hakmook Kang4,5, Ciaran M. Considine1, Manus J. Donahue1, and Daniel O. Claassen1
1Neurology, Vanderbilt University Medical Center, Nashville, TN, United States, 2Vanderbilt Brain Institute, Vanderbilt University, Nashville, TN, United States, 3Radiology and Radiological Sciences, Vanderbilt University Medical Center, Nashville, TN, United States, 4Biostatistics, Vanderbilt University Medical Center, Nashville, TN, United States, 5Center for Quantitative Sciences, Vanderbilt University Medical Center, Nashville, TN, United States

Synopsis

Keywords: Neurofluids, Alzheimer's DiseaseA pathological hallmark of Alzheimer’s disease (AD) is the elevated aggregation of protein amyloid-β (Aβ) in the cerebrum. Recent studies have suggested a role for the parasagittal dural (PSD) space in cerebrospinal fluid (CSF) egress and associated protein clearance. A fully connected neural network was used to generate PSD segmentation masks from 3D T2-weighted turbo-spin-echo data to assess the relationship between PSD space volume and Aβ burden estimated by 11C-Pittsburgh Compound B in AD participants. PSD space hypertrophy was significantly associated with elevated Aβ levels and was localized to the frontal and parietal subsegments of the PSD.

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