The relationship between disease-specific psychosocial stressors and depressive symptoms in Huntington’s disease

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Abstract

Background: Huntington’s disease (HD) is an inherited neurodegenerative disease involving motor abnormalities, cognitive decline, and psychological difficulties. Depression is among the most common psychological difficulties in HD. People with HD encounter numerous stressors related to their diagnosis and the impact of HD on their daily lives. Understanding the relationship between HD-specific psychosocial stressors and depression symptoms is critical for optimising treatment and developing a holistic, disease-specific model of depression in HD. Methods: Fifty-seven adults with the HD gene expansion (33 pre-symptomatic, 24 symptomatic) completed a self-report depression questionnaire and rated how much stress they experienced in relation to 20 psychosocial challenges commonly associated with HD. We examined associations between depression symptoms and each stressor individually, and after clustering using principal components analysis. Results: Depression symptoms were significantly associated with most of the psychosocial stressors assessed. Clustering with principal components analysis revealed that higher depression scores had significant independent associations with greater stress related to the future implications of HD (β =.44, p =.001) and sleep and psychological difficulties (β =.28, p =.005), but not with stress related to functional limitations (β =.11, p =.33) or interpersonal issues caused by HD (β =.15, p =.21). Conclusions: Stressful experiences associated with HD constitute an important risk factor for depression in HD. Our findings support the use of more psychologically informed models of depression in HD and necessitate further research on tailored psychosocial interventions for HD patients with depression.

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Bilal, H., Harding, I. H., & Stout, J. C. (2024). The relationship between disease-specific psychosocial stressors and depressive symptoms in Huntington’s disease. Journal of Neurology, 271(1), 289–299. https://doi.org/10.1007/s00415-023-11982-x

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