In Vivo Mapping of Tauopathy in Temporal Lobe Epilepsy
Abstract number :
1.124
Submission category :
2. Translational Research / 2C. Biomarkers
Year :
2022
Submission ID :
2204412
Source :
www.aesnet.org
Presentation date :
12/3/2022 12:00:00 PM
Published date :
Nov 22, 2022, 05:24 AM
Authors :
Raúl Rodríguez-Cruces, PhD – McGill University; Jessica Royer, PsyD – McGill University; Hans Auer, BSc – McGill University; Oualid Benkarim, PhD – McGill University; Jordan DeKraker, PhD – McGill University; Donna Gift Cabalo, BSc, MSc – McGill University; Alexander Ngo, BSc – McGill University; Sara Lariviere, PhD – McGill University; Shahin Tavakol, MSc – McGill University; Lorenzo Caciagli, PhD – McGill University; Birgit Frauscher, MD, PhD – McGill University; Matthias J. Koepp, MD, PhD – University College London; Andrea Bernasconi, MD, PhD – McGill University; Neda Ladbon-Bernasconi, MD, PhD – McGill University; Boris Bernhardt, PhD – McGill University
This abstract has been invited to present during the Broadening Representation Inclusion and Diversity by Growing Equity (BRIDGE) poster session
Rationale: Temporal lobe epilepsy (TLE), the most common drug-resistant epilepsy in adults, is associated with atrophy beyond the primary mesiotemporal substrate. Although TLE is traditionally not considered a neurodegenerative disorder, emerging evidence from ex vivo specimens have shown elevated levels of misfolded tau protein, a hallmark of neurodegeneration (Tai et al. 2016). In this study, we assessed the in-vivo presence of tau-aggregates in TLE using F18-MK6240, a recently validated in vivo positron emission tomography (PET) tracer and examined its associations to structural atrophy.
Methods: We included 14 drug-resistant TLE patients (median ± IQR age 33.0±4.0 years, 3 females; 3/14 had two scans available), and 15 age-and sex matched healthy controls (30.5±8.8; 4 females, 1/15 had two scans available). F18-MK6240 PET uptake was partial volume corrected, normalized for cerebellar gray matter uptake to obtain a standardized uptake value ratio, and co-registered to cortical/subcortical surfaces derived from T1-weighted 3T MRI. This resulted in vertex-wise cortical, hippocampal, and subcortical maps of tau uptake, and grey matter thickness/volume. We compared TLE and controls at the level of F18-MK6240 uptake and thickness/volume using a mixed effects model, controlling for age and sex, and corrected for multiple comparisons with random field theory (p < 0.05). To assess associations between atrophy and tau-uptake, we re-ran the mixed effects model controlling for regional grey matter thickness/volume estimates.
Translational Research