F059 Association between cognitive performance and functional capacity in Huntington’s disease
Year: 2024
Type: conference-paper
Abstract: Background 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. Methods 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. Results 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<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<0.05 for all in logistic models) figure 1. Conclusions 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. References Marder K. et al. Neurology 2000;54(2):452–8. DOI 10.1212/wnl.54.2.452. Watkins K, et al. J-Huntingtons Dis 2018;7(4):367–377. DOI 10.3233/JHD-180296. Ross CA, et al. Mov-Disord 2014;29(11):1351–8. DOI 10.1002/mds.26012. Rosenblatt A, et al. Mov-Disord 2011;26(9):1711–6. DOI 10.1002/mds.23716. Carlozzi N, et al. Mov-Disord 2019;34(12):1910–1914. DOI 10.1002/mds.27866. Horta-Barba, et al. J-Neurol 2022;269(7):3541–3549. DOI 10.1007/s00415-021-10955-2. Lunven M, et al. Brain-Commun 2023;5(2):fcad043. DOI 10.1093/braincomms/fcad043. Mov Disord 1996;11(2):136–42. DOI 10.1002/mds.870110204.
Language: English
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: gold
OpenAlex ID: W4402374405