On the association between apathy and deficits of social cognition and executive functions in Huntington's disease

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

To investigate if executive and social cognitive dysfunction was associated with apathy in a large cohort of Huntington’s disease gene expansion carriers.

Eighty premanifest and motor-manifest Huntington’s disease gene expansion carriers (Mini-Mental State Examination score ≥ 24 and Montreal Cognitive Assessment score ≥ 19) and thirty-two controls were examined with the Lille Apathy Rating Scale (LARS), a tailored and quantitative measure of apathy, and a comprehensive cognitive battery on executive functions and social cognition (emotion recognition, theory of mind and sarcasm detection), as well as general correlates like demographic variables, and neuropsychiatric and cognitive screening tests.

The motor-manifest Huntington’s disease gene expansion carriers had significantly different scores on most measures of social cognition and executive functions, compared to premanifest and control participants. Apathy was significantly correlated with most executive test scores, but the Emotion Hexagon was the only social cognitive test score significantly correlated with apathy. We found that the motor score and the depression score were the only significant predictors of the apathy score, when the social cognitive and executive tests with the strongest association with the global LARS score were entered into a multiple stepwise regression model. No cognitive test score could significantly predict apathy. The model explained 21 % of the total variance.

Despite being significantly correlated with apathy neuropsychological variables did not have a significant impact on apathy when variables as depression and motor symptoms were taken into account. Apathy should be considered an independent symptom of Huntington’s disease that requires specific examination.
TidsskriftJournal of the International Neuropsychological Society
Udgave nummer4
Sider (fra-til)369-376
Antal sider8
StatusUdgivet - 2023

Bibliografisk note

Funding Information:
This work was supported by the Danish Huntington’s Disease Association Research Fund; the A. P. Møller Foundation for the Advancement of Medical Science; the Søren Segel & Johanne Wiibro Segel’s Research Fund; The Novo Nordisk Foundation (Grant number: NNF11OC1014514); and the Research Board at Rigshospitalet.

Publisher Copyright:
© 2022 INS. Published by Cambridge University Press.

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