eNOS phosphorylation in platelets from HD patients and healthy controls.

<p><b>(A)</b> Representative immunoblotting of eNOS phosphorylation at serine residue 1177 in platelets and densitometric analysis for p-eNOS⁽¹¹⁷⁷⁾ and eNOS (left) and for eNOS and β-actin (right). <b>(B)</b> Bar graph showing endothelial NOS activity in platelets from early (I-II) and late (III-IV) stage HD patients and healthy controls. Young Ctrl n = 5; Old Ctrl n = 4; Early stage n = 9; Late stage n = 9. Data are shown as mean ± SD. *, <i>p</i> <0.05. (One-way ANOVA followed by Tukey post test). F  = 8.766; df = 26.</p

Demographic and clinical data of healthy controls and HD patients.

<p>Values are given as mean ± s.d.; TFC: Total Functional Capacity, score 13-0.</p

Vasorelaxant response to supernatants derived from insulin-stimulated platelets of HD patients.

<p>(<b>A</b>) Dose–response curves of phenylephrine-precontracted aorta rings to supernatants derived from insulin-stimulated and unstimulated platelets isolated from control subjects untreated and pre-treated with L-NAME. * indicates statistical significance of either Ctrls vs L-NAME-treated Ctrls or vs unstimulated samples. Ctrl n = 4; L-NAME-treated Ctrls n = 4; Unstimulated n = 4. (<b>B</b>) Dose–response curves of phenylephrine-precontracted aorta rings to supernatants derived from insulin-stimulated platelets isolated from early HD patients and young control subjects. Young Ctrl n = 13; Early HD n = 8. (<b>C</b>) Dose–response curves of phenylephrine-precontracted aorta rings to supernatants derived from insulin-stimulated platelets isolated from late HD patients and old control subjects. * indicates statistical significance of old Ctrl vs late HD. Old Ctrl n = 6; Late HD n = 7. (<b>D</b>) Dose–response curves of phenylephrine-precontracted aorta rings to supernatants derived from platelets isolated from Old control subjects and late HD patients untreated and pre-treated with TEMPOL before insulin stimulation. Old Ctrl n = 3; Late HD plus Tiron n = 4. * indicates statistical significance of old Ctrl vs late HD stages treated and untreated with TEMPOL. Values are shown as mean± SEM. *, <i>p</i><0.05; **, <i>p</i> <0.001; ***, <i>p</i> <0.0001. <b>(</b>Two-way ANOVA followed Bonferroni post-test<b>).</b></p

Corpus Callosum Tract Measures by Diagnosis.

<p>Bar graphs show differences between CC FA, AD, and RD for the whole CC and the seven components of the CC as defined by the tract target region. The error bars represent the Standard Error Mean (SEM). Tracts: Whole corpus callosum (CC); orbital frontal (OF), anterior frontal (AF), superior frontal (SF), superior parietal (SP), posterior parietal (PP), temporal (Temp), and occipital (Occ).</p

Significant Correlations between Corpus Callosum FA, RD and CAG Repeat Length, Disease Burden, UDRS1 & UDRS2.

<p>Significant Correlations between Corpus Callosum FA, RD and CAG Repeat Length, Disease Burden, UDRS1 & UDRS2.</p

Tractography Group Comparisons.

<p>HD = Huntington’s disease; Pre-HD = gene-positive, without motor symptoms.</p><p><b>In bold:</b> significant results after correction for multiple comparisons (FDR p<0.05).</p