Impaired brain perfusion and cerebrovascular reactivity in the zQ175 mouse model of Huntington’s Disease, a longitudinal pCASL-MRI study
Tamara Vasilkovska 1,2, Verdi Vanreusel1, Somaie Salajeghe1, Johan van Audekerke1,2, Lydiane Hirschler3, Dorian Pustina4, Roger Cachope4, Haiying Tang4, Longbin Liu4, Celia Dominguez4, Ignacio Munoz-Sanjuan4, Annemie Van der Linden1,2, and Marleen Verhoye1,2
1Bio-Imaging Lab, University of Antwerp, Antwerp, Belgium, 2µNEURO Research Centre of Excellence, University of Antwerp, Antwerp, Belgium, 3C.J. Gorter Center for High Field MRI, Leiden University Medical Center, Leiden, Netherlands, 4CHDI Management/CHDI Foundation, Princeton, NJ, United States
Abnormal cerebral vasculature and consequent diminished cerebrovascular function have been shown to play a role in Huntington’s Disease (HD). However, how these impairments reflect on cerebral blood flow (CBF) dynamics and vascular reactivity (CVR) have been poorly understood. Towards this, we performed a longitudinal study measuring CBF and CVR, using pCASL, in the zQ175 KI Huntington’s disease (HD) mouse model at pre-manifest (3/4.5 months), disease onset (6 months) and manifest (9 months) stage. Our results demonstrate decreased CBF under CO2 challenge at disease onset and decreased CVR in manifest HD stage in the zQ175 KI mice compared to age-matched controls.
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