The vascular depression hypothesis posits that there is a relationship between vascular disease and geriatric depressive symptoms. Black Americans are at higher risk for cardiovascular disease (CVD) than their White counterparts. However, it is not fully understood whether risk for CVD or potentially related neurovascular changes have a differential relationship in Black and White Americans. We investigated differences in the relationships between white matter hyperintensities, risk for CVD, and depressive symptoms in Black and White older adults.

Participants were derived from the National Alzheimer Coordinating Center database. Black (N = 120) and White (N = 120) participants were matched on age, sex, and education. White matter hyperintensity (WMH) and CVD burden data (sum of vascular conditions) on 320 individuals were analyzed (mean age = 75.9; 69.4% female). Age, sex, race, and education were included as covariates in separate regression models in which WMH and CVD burden predicted scores on the 15-item Geriatric Depression Scale (GDS-15). Follow-up stratified analyses were conducted to explore the relationship between WMH and CVD burden on GDS scores in the Black and White samples.

Lower WMH volume and higher CVD burden were associated with higher GDS scores in the total sample. Analyses stratified by race showed a positive effect of CVD burden on GDS scores only for the Black sample and a trend effect of WMH on GDS scores only for the White sample, with higher WMH volume associated with lower rather than higher GDS scores.

These findings are consistent with previous research showing that WMH and CVD burden are related to depression in older adults. Contrary to expectation, WMH had a negative trend association with GDS scores in the White sample. Findings also suggest that different etiologies may play a role in the clinical presentation of depression in Black and White Americans. Additional research is needed to further explore the relationships among CVD, its neural correlates, and depressive symptoms in diverse samples.

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.