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Depressive symptom severity is related to poorer cognitive performance in prodromal Huntington disease
Megan M Smith1, James A Mills, Eric A Epping
1Carver College of Medicine, University of Iowa, Iowa City, IA, USA.
Insights
Depression severity is linked to worse cognitive function in individuals with prodromal Huntington disease (HD). Addressing depression may improve cognitive impairment in HD patients.
Area of Science:
- Neuroscience
- Psychiatry
- Genetics
Background:
- Huntington disease (HD) is a neurodegenerative disorder.
- Depression is common in HD and may worsen cognitive deficits.
- Research on depression's impact on cognition in prodromal HD is limited.
Purpose of the Study:
- To investigate the relationship between depressive symptom severity and cognitive performance in individuals with prodromal HD.
- To examine executive functioning, learning/memory, and attention in relation to depression levels.
Main Methods:
- 814 prodromal HD participants and 230 gene-negative controls completed neuropsychological tests.
- The Beck Depression Inventory-II (BDI-II) assessed depression severity.
- Participants were categorized into minimal, mild, moderate, and severe depression groups based on BDI-II scores.
Main Results:
- Moderate and severe depression groups performed worse on tests of executive functioning (SDMT, Trails B, Stroop interference) and learning/memory (HVLT-R Immediate Recall) compared to minimal and mild groups.
- Depression severity and gene status significantly predicted cognitive performance.
- Gene status had a greater impact on memory and Trails B performance, while depression and gene status had comparable contributions to other cognitive tests.
Conclusions:
- Depressive symptom severity is associated with poorer cognitive performance in prodromal HD.
- Depression may be a treatable factor contributing to cognitive impairment in this population.
- Findings suggest potential therapeutic targets for cognitive deficits in HD.
Objective:
Depression is associated with more severe cognitive deficits in many neurological disorders, though the investigation of this relationship in Huntington disease (HD) has been limited. This study examined the relationship between depressive symptom severity and measures of executive functioning, learning/memory, and attention in prodromal HD.
Method:
Participants (814 prodromal HD, 230 gene-negative) completed a neuropsychological test battery and the Beck Depression Inventory-II (BDI-II). Based on the BDI-II, there were 637 participants with minimal depression, 89 with mild depression, 61 with moderate depression, and 27 with severe depression in the prodromal HD group.
Results:
ANCOVA (controlling for age, sex, and education) revealed that performance on SDMT, Trails B, Hopkins Verbal Learning Test--Revised (HVLT-R) Immediate Recall, and Stroop interference was significantly different between the BDI-II severity groups, with the moderate and severe groups performing worse than the minimal and mild groups. There were no significant differences between the BDI-II severity groups for Trails A or HVLT-R Delayed Recall. Linear regression revealed that both gene status and depression severity were significant predictors of performance on all cognitive tests examined, with contributions of BDI-II and gene status comparable for Trails A, SDMT, and Stroop interference. Gene status had a higher contribution for HVLT-R Immediate and Delayed Recall and Trails B.
Conclusions:
Our results suggest that depressive symptom severity is related to poorer cognitive performance in individuals with prodromal HD. Though there are currently no approved therapies for cognitive impairment in HD, our findings suggest that depression may be a treatable contributor to cognitive impairment in this population.
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