Apathy and Functional Status in Early-Stage Huntington’s Disease
Publication: The Journal of Neuropsychiatry and Clinical Neurosciences
Abstract
Objective:
Apathy is common in Huntington’s disease (HD) and difficult to treat. Multiple recent calls have been made to increase understanding of apathy across the spectrum of HD severity. Functional status is an important outcome in HD trials; however, no consensus currently exists regarding the impact of apathy on functional status in HD. The authors aimed to identify correlates of apathy and effects on functional status in a primarily early-stage HD sample.
Methods:
This study included secondary analyses of data from a study of neuropsychiatric symptoms in a clinical HD sample. Spearman correlation analyses were used to assess the relationships between apathy (with the Frontal Systems Behavior Scale–Apathy [FrSBe-Apathy] subscore), clinical variables, and patient-reported outcomes. To assess the association of apathy with functional status, two multiple regression analyses were performed, with a different functional status measure (Adult Functional Adaptive Behavior [AFAB] scale or Total Functional Capacity [TFC] scale) as the dependent variable in each analysis.
Results:
Statistically significant correlates of apathy included the Quality of Life in Neurological Disorders (Neuro-QoL) Satisfaction With Social Roles and Activities and Neuro-QoL Positive Affect and Well-Being scores (N=70 patients). Univariate correlation analyses also revealed statistically significant associations of FrSBe-Apathy scores with both functional status measures. In the multiple regression analyses, apathy significantly contributed to variability in functional status as measured by both the AFAB (N=49 patients) and TFC (N=56 patients) scales.
Conclusions:
These results underscore the need to address apathy as a target for improving functional status, social satisfaction, and well-being in HD, even for individuals with early-stage HD.
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Information & Authors
Information
Published In
The Journal of Neuropsychiatry and Clinical Neurosciences
History
Received: 20 December 2023
Revision received: 16 May 2024
Accepted: 17 May 2024
Published online: 19 November 2024
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Authors
Competing Interests
The content of this article is solely the responsibility of the authors and does not necessarily represent the official views of the NIH or the authors’ institutions.
Dr. Gibson reports receiving consulting fees from Teva Pharmaceuticals. Dr. Claassen reports receiving research support from the Griffin Family Foundation and the Huntington Disease Society of America; pharmaceutical grant support from AbbVie, Acadia, Alterity, Biogen, BMS, Cerecour, Eli Lilly, Genentech-Roche, Jazz Pharmaceuticals, Lundbeck, Neurocrine, Teva Neuroscience, UniQure, Vaccinex, and Wave Life Sciences; and consulting fees from Acadia, Adamas, Alterity, Anexon, Ceruvel, Lundbeck, Neurocrine, Spark, Teva Neuroscience, and UniQure. Dr. Brown reports receiving research support from CHDI Foundation and Parkinson’s Foundation; pharmaceutical grant support from AbbVie, Alterity Therapeutics, Amylyx Pharmaceuticals, Genentech-Roche, Neurocrine Biosciences, Novartis, Orphalan, PTC Therapeutics, Sage Therapeutics, Teva Neuroscience, and UniQure; and consulting fees from Orphalan. Dr. Isaacs reports receiving research funding from Teva Neuroscience and the Tourette Association of America. The other authors report no financial relationships with commercial interests.
Funding Information
This study was supported by an iTHRIV Scholar Award from the University of Virginia (grant UL1TR00315/KL2TR003016 to Dr. Gibson), the National Institute of Nursing Research (grant K23NR020210 to Dr. Gibson), an investigator-initiated grant from Teva Neuroscience (to Dr. Isaacs), the National Center for Advancing Translational Sciences (grant UL1 TR002243 to Dr. Isaacs), and the National Institute of Neurological Disorders and Stroke (grant K23NS131592 to Dr. Isaacs).
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