Protein aggregates containing wild-type and mutant NOTCH3 are major drivers of arterial pathology in CADASIL.

Although this difference did not reach statistical significance using a linear mixed model, employed to assess the interdependence of measurements of distinct SMCs from the same animal ( Figure 9, B–D ), we found a significant leftward shift in the mean intensity distribution of aggregates in Tg Notch3 R169C Notch3 +/– mice ( Figure 9E ).

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Quantitative immunofluorescence analyses showed a trend toward a reduction in the number of aggregates in arterial SMCs of Tg Notch3 R169C Notch3 +/– mice compared with Tg Notch3 R169C Notch3 +/+ mice ( Figure 9A and Supplemental Figure 8 ).

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