Abstract Details

Title White matter hyperintensities in frontotemporal lobar degeneration

Topic Aging, Dementia, and Behavioral Neurology

Presentation(s) P1 - Poster Session 1 (9:00 AM-5:00 PM)

Poster/Presentation
Number 030

Objective

To characterize the prevalence of white matter hyperintensities (WMH) and their associated phenotype and pathology in a sporadic cohort of frontotemporal lobar degeneration (FTLD) patients.

Background A variety of pathologies can lead to increased WMH burden, including vascular disease and Alzheimer's disease (AD)-associated neurodegeneration. In the context of sporadic FTLD neither the aetiology (risk factors, associated pathology), nor the effects of WMH pathology are well-understood.

Design/Methods Data were pooled from three multi-site datasets (Local/FTLDNI/4RTNI) and included 119 healthy controls, 55 behavioural variant frontotemporal dementia (bvFTD), 25 progressive non-fluent aphasia (PNFA), 37 semantic variant primary progressive aphasia (svPPA), 45 corticobasal syndrome (CBS), and 48 progressive supranuclear palsy (PSP) patients. The LPA toolbox was used to obtain binary WMH maps from FLAIR scans and the logged total WMH volume was used in statistical analyses. The CAT12 toolbox was used for T1-w image segmentation. For a subset of 36 patients, medical history, Alzheimer's disease pathology (CSF), and axonal damage (CSF neurofilament light chain level) were further examined in relation to WMH volume.

Results The average raw WMH volume in the FTLD clinical subtypes varied from 6.76 mL (svPPA) to 14.9 mL (bvFTD) and all groups had significantly increased WMH volume compared to the control group (2.27mL) (p<0.001), after accounting for the effect of age (p<0.001), gender (p>0.05), and site (p<0.001). The bvFTD patients had significantly higher levels of WMH than all other FTLD clinical subtypes (p<0.05). There was no difference in WMH volume between patients who reported at least one vascular risk factor versus none, nor in relation to AD biomarker status (p>0.05).

Conclusions All FTLD clinical variants present considerably high volumes of WMH, particularly the bvFTD and CBS groups. Our preliminary data suggest WMH load in FTLD is not explained by the typical vascular or AD-related pathology, and further investigation into its cause is ongoing.

Authors/Disclosures
Chloe Anastassiadis (Tanz Centre for Research on Neurodegenerative Disease) PRESENTER	Ms. Anastassiadis has received research support from Fonds de Recherche du Québec - Santé (FRQS).
Anna Vasilevskaya, PhD	Anna Vasilevskaya has nothing to disclose.
Foad Taghdiri, MD, MSc (University of Toronto)	Dr. Taghdiri has nothing to disclose.
	No disclosure on file
Carmela Tartaglia, MD (Toronto Western Hospital, University of Toronto)	Dr. Tartaglia has received personal compensation in the range of $0-$499 for serving on a Scientific Advisory or Data Safety Monitoring board for Roche. The institution of Dr. Tartaglia has received research support from NIH. The institution of Dr. Tartaglia has received research support from University of Toronto.

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