Abstract #0976

Impaired oxygen metabolism in the brain during visual stimulation in premanifest Huntington's Disease patients detected by 3D-TRIP MRI at 7T

Peter Klinkmueller^1,2,3, Martin Kronenbuerger^4,5, Xinyuan Miao^2,3, Russell L. Margolis⁵, Peter C. M. van Zijl^2,3, Christopher A. Ross^4,5,6, and Jun Hua^2,3

¹Department of Electrical and Computer Engineering, Johns Hopkins University, Baltimore, MD, United States, ²F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, Baltimore, MD, United States, ³Division of MRI Research, Department of Radiology, Johns Hopkins University School of Medicine, Baltimore, MD, United States, ⁴Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, United States, ⁵Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, United States, ⁶Department of Neuroscience and Pharmacology, Johns Hopkins University School of Medicine, Baltimore, MD, United States

Huntington’s disease (HD) is a neurodegenerative disease caused by a single genetic mutation. Neurovascular abnormalities have been implicated in the pathophysiology of HD. Here, dynamic responses in BOLD, cerebral-blood-flow (CBF) and -volume (CBV) during visual stimulation were measured using 3D-TRiple-acquisition-after-Inversion-Preparation (3D-TRIP) MRI in premanifest HD patients and healthy controls, from which cerebral-metabolic-rate-of-oxygen (CMRO₂) response was estimated. Decreased ΔCMRO₂ and increased ΔCBV were observed in HD patients compared to controls, which correlated with genetic measures. The results suggested potential value of ΔCMRO₂ as a biomarker for HD, and may shed light on the pathophysiology in HD in terms of mitochondrial deficiency.

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