F059 Association between cognitive performance and functional capacity in Huntington’s disease

<h3>Background</h3> In Huntington’s disease (HD) individuals experience limitations in work-related activities (WRAs) as well as in executing basic and instrumental activities of daily living (ADLs and IADLs) even before the onset of motor symptoms[1–5]. However, the contribution of cognitive decline indistinctly of motor symptoms remains unclear[3, 6]. Aims to identify cognitive domains associated with limitations in daily living in people with HD, while isolating cognitive processing times from motor response times. <h3>Methods</h3> This study included all BioHD and RepairHD HD participants with data from the SelfCog inverted efficiency score (IES)[7] and the UHDRS cognitive performance and functional limitations tests[8]. Adjusted linear models were calibrated between functional assessments and cognitive tests (figure 1). Psychometric screening of ADLs, IADLs and WRAs was performed, and a logistic model fitted between ADLs, IADLs, WRA dependence and cognitive domains was calibrated. <h3>Results</h3> Analysis adjusted to motor-related factors in 158 participants (43% females) with mean age to 51.12(11.5) showed that global and executive cognitive decline were strongly associated with declining functional capacity (p&lt;0.001 in lineal models). The comparison coefficients using normalized scores revealed that global IES and executive IES displayed higher coefficients than those using the UHDRS cognitive test. A low global and executive cognitive performance may be associated to ADL, IADL and WRA dependency (OR=1.6–2.88, p&lt;0.05 for all in logistic models) figure 1. <h3>Conclusions</h3> Our findings suggest that the loss of functional capacity in the HD population is associated with cognitive decline. The decline in executive function performance may be a marker of loss of autonomy in IADLs and WRAs. <h3>References</h3> Marder K. <i>et al. Neurology</i> 2000;<b>54</b>(2):452–8. DOI 10.1212/wnl.54.2.452. Watkins K, <i>et al. J-Huntingtons Dis</i> 2018;<b>7</b>(4):367–377. DOI 10.3233/JHD-180296. Ross CA, <i>et al. Mov-Disord</i> 2014;<b>29</b>(11):1351–8. DOI 10.1002/mds.26012. Rosenblatt A, <i>et al. Mov-Disord</i> 2011;<b>26</b>(9):1711–6. DOI 10.1002/mds.23716. Carlozzi N, <i>et al. Mov-Disord</i> 2019;<b>34</b>(12):1910–1914. DOI 10.1002/mds.27866. Horta-Barba, <i>et al. J-Neurol</i> 2022;<b>269</b>(7):3541–3549. DOI 10.1007/s00415-021-10955-2. Lunven M, <i>et al. Brain-Commun</i> 2023;<b>5</b>(2):fcad043. DOI 10.1093/braincomms/fcad043. <i>Mov Disord</i> 1996;<b>11</b>(2):136–42. DOI 10.1002/mds.870110204.