Abstract Details

Title Asymmetrical Brain Atrophy in Huntington's Disease: A Post Mortem MRI Study

Topic Movement Disorders

Presentation(s) P10 - Poster Session 10 (5:00 PM-6:00 PM)

Poster/Presentation
Number 5-026

Objective In this study, we aim to characterize region-specific gray and white matter differences between Huntington's Disease (HD) patients and controls.

Background Huntington’s Disease is a progressive, autosomal dominant, neurodegenerative disease caused by a CAG repeat expansion in the HTT gene. Medium spiny neurons of the striatum are especially vulnerable to the disease, and atrophy of the caudate and putamen can be documented by neuroimaging years before the onset of symptoms.

Design/Methods We conducted a post-mortem MRI study of the brains of 15 adults diagnosed with symptomatic Huntington’s Disease and 26 control subjects, aiming to compare the differences in regional grey and white matter volumes between the two groups.

Results The study revealed decreased volumes in both grey and white matter in patients with Huntington’s Disease, with the largest effect sizes observed in caudate and putamen. Notably, the atrophy predominantly affected the left hemisphere, particularly impacting grey and white matter regions adjacent to the pars opercularis, precentral, supramarginal, and pars orbitalis gyri, and the lateral orbitofrontal cortex. In the control group, asymmetry stems from larger left hemisphere regions compared to right, whereas an opposite pattern is observed in the Huntington’s Disease group.

Conclusions These results suggest progressive, diffuse, and asymmetrical grey and white matter atrophy occurs in Huntington’s Disease. The reasons for this asymmetry remain unknown; however, our study provides a more detailed characterization of previously reported grey and white matter changes in Huntington's Disease, as observed through post-mortem histopathological and MRI studies. Similar findings have been noted in other neurodegenerative diseases, such as frontotemporal dementia, primary progressive aphasia, and possibly Alzheimer's disease.

Authors/Disclosures
Bianca Le, MA-P (University of Washington) PRESENTER	Ms. Le has nothing to disclose.
Eardi Lila, PhD	Dr. Lila has nothing to disclose.
David Hunt, PhD	Dr. Hunt has nothing to disclose.
Daniel D. Child, MD, PhD	Dr. Child has nothing to disclose.
Caitlin S. Latimer, MD, PhD	Dr. Latimer has nothing to disclose.
Marie Y. Davis, MD, PhD (VA Puget Sound)	Dr. Davis has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Biogen. The institution of Dr. Davis has received research support from NIH NINDS. The institution of Dr. Davis has received research support from University of Washington Institute for Stem Cell and Regenerative Medicine. The institution of Dr. Davis has received research support from VA BLRD. Dr. Davis has received personal compensation in the range of $500-$4,999 for serving as a study section grant reviewer with NIH. Dr. Davis has received personal compensation in the range of $500-$4,999 for serving as a Grant reviewer with Parkinson's Foundation.
Suman Jayadev, MD (University of Washington Medical Center)	Dr. Jayadev has nothing to disclose.
Thomas D. Bird, MD, FAAN	Dr. Bird has nothing to disclose.
Ali Shojaie, PhD	Prof. Shojaie has nothing to disclose.
Christine MacDonald, PhD (University of Washington)	The institution of Dr. MacDonald has received research support from NIH. The institution of Dr. MacDonald has received research support from Department of Defense.

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