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 Song^1,2, Kilian Hett¹, Jarrod J. Eisma¹, Colin D. Mcknight³, Jason Elenberger¹, Adam J. Stark¹, Hakmook Kang^4,5, 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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