Regardless of genetic risk, a higher Brain Care Score (BCS) mitigates the risk for stroke, late-life depression, and dementia, according to study findings published in Neurology.
Researchers used the UK Biobank prospective cohort study to determine the influence of a higher BCS on inherited genetic risk for stroke, late-life depression, and dementia among unrelated individuals of European ancestry who had available genetic data.
Primary outcomes included incident stroke, late-life depression, and dementia. To assess the associations between BCS, genetic predisposition, and the primary outcomes, multivariate Cox proportional hazard models were used.
A total of 368,340 participants (median age, 58; men, 46.3%; median BCS, 11) were included in the stroke and dementia outcome group, while 304,468 participants were included in the late-life depression outcome group.
During a median 12.5-year follow-up, a total of 9361 stroke events, 6959 new cases of dementia, and 14,371 new cases of late-life depression were observed.
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Further work is needed to prospectively investigate the utility and performance of the BCS as a targeted intervention in populations at elevated genetic risk of age-related brain disease.
Each 5-point increase in BCS at baseline was independently associated with a decreased risk for stroke (hazard ratio [HR], 0.70; 95% CI, 0.68-0.73), late-life depression (HR, 0.60; 95% CI, 0.59-0.62), and dementia (HR, 0.83; 95% CI, 0.79-0.86).
High genetic risk for stroke and lower BCS were independently associated with higher stroke risk. Independent HR of incident stroke was 73% (95% CI, 1.63-1.83) higher among those at high vs low genetic risk and 30% (95% CI, 0.68-0.73) lower by 5-point BCS increase.
Higher BCS was protective against stroke within each category of genetic risk. In those with high genetic risk, incident stroke was 1.2 per 1000 person-years among those with a high BCS and 2.8 per 1000 person-years among those with a low BCS. Among those with low genetic risk, incident stroke was 1.6 and 0.68 per 1000 person-years for those with a high and low BCS, respectively.
For late-life depression, an increase of 5 points in BCS was associated with a 35% (95% CI, 0.63-0.67) lower risk for the outcome, independent of genetic risk. A high BCS was associated with 54% lower risk for late-life depression among participants at the highest (HR, 0.46; 95% CI, 0.42-0.51) and lowest (HR, 0.46; 95% CI, 0.41-0.52) genetic predisposition.
Among those at high genetic risk, the incidence of late-life depression was 4.46 per 1000 person-years for those with a high BCS and 7.34 per 1000 person-years for those with a low BCS. Standardized incidence rates among those at low genetic risk were 3.17 and 4.58 per 1000 person-years for those with high and low BCS, respectively.
A difference of 5 points in BCS was associated with an 18% lower risk for dementia, independent of APOE status (HR, 0.82; 95% CI, 0.79-0.86). A statistically significant interaction between high genetic risk and BCS (HR, 1.25; 95% CI, 1.14-1.36) was observed.
Among those with high genetic dementia risk, dementia incidence was 2.05 per 1000 person-years for those with high BCS and 3.64 per 1000 person-years for those with low BCS.
Study limitations include the observational design of the UK Biobank study, potential selection bias, and reduced generalizability of results to more diverse patient populations.
“Further work is needed to prospectively investigate the utility and performance of the BCS as a targeted intervention in populations at elevated genetic risk of age-related brain disease,” the study authors concluded.
Disclosure: One study author declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures.