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Several studies have noted associations of higher white matter hyperintensities (WMHs) with cognitive slowing and elevated depressive symptoms in older adults. Depression is also directly associated with cognitive slowing in later life. However, the influence of WMHs on the relationship between depressive symptoms and processing speed is unclear. This interrelationship between depression, processing speed, and WMH may differ between racial groups given the well-documented evidence of racial disparities in vascular disease, WMHs, and cognitive performance, however the literature is sparse. The goal of this current study, therefore, was to investigate whether WMHs mediate the relationship between depressive symptoms and processing speed, and if this relationship differs between Black and White older adults.
Participants and Methods:
A total of 171 non-Hispanic White and 111 non-Hispanic Black older adults (total sample mean age = 82.71 ± 2.74; 42.91% male) from the Healthy Brain Project (a substudy of the Health, Aging, and Body Composition Study) underwent MRI as well as a neuropsychological evaluation. Total WMH volume was quantified for each participant using an automated procedure and normalized to total brain volume. Depressive symptoms were assessed using the Center for Epidemiologic Studies Depression Scale (CES-D) and the Digit Symbol Substitution Test (DSST) served as a measure of processing speed. Causal mediation analyses were performed between CES-D and DSST scores across the total sample as well as within racial groups (Black and White), with total WMH volume as the mediator.
The direct effect of the CES-D on DSST was significant (p = 0.012) for the total sample, reflecting slower processing speed at higher levels of depressive symptoms, but the indirect effect was not (p = 0.207). When analyses were stratified by racial group, the indirect effect was significant for Black (p = 0.054; 37.17% mediated) but not White participants (p = 0.207): For Black participants, the inverse relationship between depressive symptoms and processing speed was mediated by a positive relationship between depressive symptoms and WMHs.
While these data support previous findings relating depressive symptoms to slower processing speed across racial groups, our findings also demonstrate a greater impact of WMHs on this relationship in Black older adults compared to their White counterparts. This suggests that WMHs may serve as an important risk factor for cognitive slowing in older Black adults with higher depressive symptoms. Future studies are needed to further investigate the role of WMHs on depression-related deficits in processing speed and other cognitive domains in racially diverse groups.
brain white matter integrity as a result of vascular burden is associated with a form of late-life depression, known as vascular depression (VaDep). Black older adults may be particularly vulnerable to developing VaDep due to a higher prevalence of vascular conditions compared to White older adults. The current study examined whether clinical and imaging markers of vascular burden predicted depressive symptoms in an older Black sample. Based on the literature in primarily White samples, we expected greater clinical vascular burden and white matter hyperintensity (WMH) volume to predict greater depressive symptoms both cross-sectionally and over 4-year follow-up. We additionally hypothesized that participants with operationally-defined VaDep would have worse cognitive performance and slower gait speed compared to those without VaDep. Exploratory analyses examined race (Black vs. White) as an additional predictor.
Participants and Methods:
This study used publicly available data from 113 Black older adults who were followed for four years in the Healthy Brain Project (a substudy of the Health, Aging, and Body Composition Study). Clinical vascular burden was defined as the number of vascular conditions (e.g., hypertension, diabetes, stroke); total WMH volume and WMH volume in the uncinate fasciculus, superior longitudinal fasciculus, and cingulum were considered imaging markers of vascular burden. Clinical and imaging-defined vascular burden were used to predict baseline depressive symptoms and average depressive symptoms over follow-up as measured by the Center for Epidemiologic Studies Depression Scale (CES-D). We then formed groups based on cutoffs for vascular burden (two or more conditions) and depressive symptoms (upper tertile of CES-D scores) to compare cognitive (Digit Symbol Substitution Test and 15-Item Executive Interview) and gait speed performance at baseline and changes over four years in VaDep, non-vascular depression, vascular only, and healthy groups. Exploratory analyses included 179 White older adults from the Healthy Brain Project dataset to examine race differences.
Total WMH volume and WMH volume in the uncinate fasciculus predicted higher depressive symptoms both cross-sectionally and longitudinally. However, no similar pattern emerged when using clinically-defined vascular burden as the predictor. The VaDep group had the slowest processing speed but the trajectory of decline over time did not differ between groups. The non-vascular depression group’s executive performance improved over time while performance by the other groups remained stable. Both VaDep and non-vascular depression groups’ gait speed declined over time. There was a stronger association between depression and uncinate fasciculus WMH in Black compared to White individuals, and the Black VaDep group had the slowest baseline processing speed of all groups.
This research supports the validity of the VaDep framework in Black older adults by showing the impact of WMH, particularly in the uncinate fasciculus, on depressive symptoms and identifying cognitive risks associated with VaDep in this population. Moreover, results suggest WMH may confer a greater risk for depression in Black compared to White older adults, and that VaDep disproportionately impacts processing speed in Black older adults. This work addresses an important gap in the VaDep literature by examining a group that has historically been underserved.
To lay out the argument that exercise impacts neurobiological targets common to both mood and cognitive functioning, and thus more research should be conducted on its use as an alternative or adjunctive treatment for cognitive impairment in late-life depression (LLD).
This narrative review summarizes the literature on cognitive impairment in LLD, describes the structural and functional brain changes and neurochemical changes that are linked to both cognitive impairment and mood disruption, and explains how exercise targets these same neurobiological changes and can thus provide an alternative or adjunctive treatment for cognitive impairment in LLD.
Cognitive impairment is common in LLD and predicts recurrence of depression, poor response to antidepressant treatment, and overall disability. Traditional depression treatment with medication, psychotherapy, or both, is not effective in fully reversing cognitive impairment for most depressed older adults. Physical exercise is an ideal treatment candidate based on evidence that it 1) is an effective treatment for depression, 2) enhances cognitive functioning in normal aging and in other patient populations, and 3) targets many of the neurobiological mechanisms that underlie mood and cognitive functioning. Results of the limited existing clinical trials of exercise for cognitive impairment in depression are mixed but overall support this contention.
Although limited, existing evidence suggests exercise may be a viable alternative or adjunctive treatment to address cognitive impairment in LLD, and thus more research in this area is warranted. Moving forward, additional research is needed in large, diverse samples to translate the growing research findings into clinical practice.
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