E006 Ultrashort echo time magnetic resonance imaging of myelin and iron in Huntington’s disease (HD)

<h3>Background</h3> Past studies have demonstrated extensive white and gray matter degeneration in Huntington’s Disease (HD), including demyelination and iron accumulation.^1–4 Demyelination disrupts axonal transport, integrity, and structural plasticity,^5–7 and plays a major role in HD.^8–10 Iron accumulation contributes to neurodegeneration.^11–13 However, myelin has an ultrashort T2, and is ’invisible’ with conventional MRI, which provides no quantitative information on iron. <h3>Aims</h3> We report a 3D Short TR Adiabatic Inversion Recovery UTE (STAIR-UTE) sequence for Myelin Proton Fraction (MPF) mapping,¹⁴ a UTE Quantitative Susceptibility Mapping (UTE-QSM) sequence for iron mapping,¹⁵ and a divided Subtracted Inversion Recovery (dSIR) sequence¹⁶ for high contrast imaging in HD. <h3>Methods</h3> The STAIR-UTE sequence included: FOV=220×220×240 mm³, matrix=92×92×80, resoltion=2.4×2.4×4.0 mm³, TE=0.032/1.2ms, TR/TI=154/67ms, bandwidth=125 kHz, 7.5 min. The UTE-QSM sequence included: FOV=220×220×160 mm³, matrix=220×220×80, resolution=1.0×1.0×2.0 mm³, TR=28ms, six-echo (TE=0.032,4.4,8.8,13.2,17.6,22ms), 7 min. The dSIR sequence included two inversion recovery FSE acquisitions with TIs of 400/600ms. Five HD patients and five controls were scheduled (four participants already scanned) for this feasibility study. <h3>Results/Outcome</h3> Figure 1 shows MPF maps that display myelin loss in white matter of the HD patient compared with the control. Figure 2 shows UTE-QSM maps. These show significant iron accumulation in putamen, globus pallidus, caudate, and external capsule of the HD patient compared with the control. Figure 3 shows dSIR images which depict abnormal structural changes in white matter of the HD patient and smaller globus pallidus, putamen and caudate nucleus compared with the control. <h3>Conclusion</h3> STAIR-UTE, UTE-QSM, and dSIR sequences can depict myelin loss, iron accumulation, and structural changes in HD patients. <h3>References</h3> Bartzokis, <i>et al. Neurochem Res</i> 2007;<b>32</b>:1655–64. Bohanna, <i>et al. Brain Res Rev</i> 2008;<b>58</b>:209–25. Kassubek, <i>et al. CerebCortex</i> 2005;<b>15</b>:846–53. Kloppel, <i>et al. Neuroscience</i> 2009;<b>164</b>:205–19. Waxman SG. <i>ArchNeurol</i> 1977;<b>34</b>(10):585–9. Filley, <i>et al. Neurophysiol</i> 2016;<b>116</b>(5):2093–104. Miller, <i>et al. PNAS</i> 2012;<b>109</b>:16480–5. Dean,<i> et al. Neuroimage</i> 2016;<b>132</b>:225–37. Bourbon-Teles, <i>et al. J Neuroscience</i> 2019;<b>403</b>:79–92. Casella, <i>et al. J Huntington’s Dis</i> 2020;<b>9</b>:303–20. Chen, <i>et al. JNR</i> 2019;<b>97</b>:467–79. Dominguez, <i>et al. JNNP</i> 2016;<b>87</b>:545–9. van Bergen, <i>et al. AJNR</i> 2016;<b>37</b>:789–96. Ma, <i>et al. Radiology</i> 2020;<b>297</b>:392–404. Jang, <i>et al. Front Neurosci</i> 2022;<b>16</b>:1033801. Ma, <i>et al. QIMS</i> 2023;<b>13</b>:7304–7337.