Regardless of genetic risk, a higher Brain Care Score (BCS) attenuates the risk of stroke, late-life depression and dementia, according to the results of a study published in Neurology.
Researchers used the UK Biobank prospective cohort study to determine the influence of higher BCS on the inherited genetic risk of stroke, late-life depression, and dementia in unrelated individuals of European ancestry who had genetic data.
Primary outcomes included stroke, late-life depression and dementia. To assess associations between BCS, genetic predisposition and primary outcomes, multivariate Cox proportional hazard models were used.
A total of 368,340 participants (median age, 58 years; male, 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 follow-up of 12.5 years, a total of 9,361 strokes, 6,959 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 BCS as a targeted intervention in populations at high genetic risk for age-related brain disease.
Each 5-point increase in BCS at baseline was independently associated with a decreased risk of stroke (hazard ratio (HR), 0.70; 95% CI, 0.68-0.73), depression in end of life (HR, 0.60; 95% CI, 0.59). -0.62) and dementia (HR, 0.83; 95% CI, 0.79-0.86).
Higher genetic risk of stroke and lower BCS were independently associated with higher risk of stroke. Stroke-independent HR was 73% (95% CI: 1.63-1.83) higher in those with high or low genetic risk and 30% (95% CI: 0.68) -0.73) lower than a 5 point increase in BCS.
Higher BCS protected against stroke in each genetic risk category. Among people at high genetic risk, stroke was 1.2 per 1,000 person-years among those with high BCS and 2.8 per 1,000 person-years among those with low BCS. Among those at low genetic risk, strokes were 1.6 and 0.68 per 1,000 person-years for those with high and low BCS, respectively.
For late-life depression, a 5-point increase in BCS was associated with a 35% lower risk (95% CI, 0.63-0.67), independent of genetic risk. High BCS was associated with a 54% lower risk of late-life depression among participants with the highest genetic predisposition (HR, 0.46; 95% CI, 0.42-0.51) and lower (HR, 0.46; 95% CI, 0.41-0.52). .
Among those at high genetic risk, the incidence of late-life depression was 4.46 per 1,000 person-years for those with high BCS and 7.34 per 1,000 person-years for those with a low BCS. The standardized incidence rates among those with low genetic risk were 3.17 and 4.58 per 1,000 person-years for those with high and low BCS, respectively.
A 5-point difference in BCS was associated with an 18% lower risk of 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 people at high risk of genetic dementia, dementia the 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.
Limitations of the study include the observational design of the UK Biobank study, potential selection bias, and reduced generalizability of results to more diverse patient populations.
“Additional work is needed to prospectively investigate the utility and performance of BCS as a targeted tool. intervention in populations at high genetic risk for age-related brain disease,” the study authors concluded.
Disclosure: One study author declared affiliations with biotechnology, pharmaceutical, and/or device companies. Please see the original reference for a complete list of author disclosures.