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Abstract #4227

Detection of amyloid-related imaging abnormality (ARIA) in Alzheimer’s patients receiving anti-amyloid antibody therapy using long-TE ASL MRI

Zhiyi Hu1, Chenyang Li2, Zihan Wang1, Li Jiang2, Thomas Wisniewski3,4, Yulin Ge2, and Hanzhang Lu1,5,6
1Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, United States, 2Department of Radiology, Center for Biomedical Imaging, New York University Grossman School of Medicine, New York, NY, United States, 3Department of Neurology, Center for Cognitive Neurology, New York University Grossman School of Medicine, New York, NY, United States, 4Alzheimer's Disease Research Center, New York University Grossman School of Medicine, New York, NY, United States, 5The Russell H. Morgan Department of Radiology & Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD, United States, 6F. M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Research Institute, Baltimore, MD, United States

Synopsis

Keywords: Alzheimer's Disease, Alzheimer's Disease

Motivation: Anti-amyloid antibody therapy has brought excitement to the Alzheimer’s community but the common side-effect of amyloid-related imaging abnormality (ARIA) related to small vessel damage still represents a major caveat.

Goal(s): To conduct early detection of ARIA using long-TE arterial-spin labeling (ASL) MRI.

Approach: Three Alzheimer’s patients were studied. ASL CSF fraction maps were obtained using a long-TE ASL with effective TE (eTE)=480ms. Three healthy volunteers were also studied.

Results: Regions with brain lesions or ARIA-E revealed higher ASL CSF fraction when compared to the rest of the brain. ASL CSF fraction in deep-brain was higher in patients than in controls.

Impact: This study demonstrated the first application of long-TE ASL in AD patients receiving anti-amyloid antibody therapy. The results support the hypothesis that arterial vessels are leaky following anti-amyloid therapy, presumably due to clearance of amyloid beta (Aβ) from vessel walls.

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