Nurturing Your Brain: How Healthy Habits Shield Mental Vitality

Irrespective of genetic predisposition, an elevated Brain Care Score (BCS) reduces the likelihood of stroke, late-life depression, and dementia, according to research findings published in Neurology.

Researchers utilized the UK Biobank prospective cohort study to examine the effect of an increased BCS on genetic risk for stroke, late-life depression, and dementia among unrelated individuals of European descent who had accessible genetic data.

Key outcomes encompassed incident stroke, late-life depression, and dementia. To evaluate the relationships among BCS, genetic inclination, and the primary outcomes, multivariate Cox proportional hazards models were employed.

A total of 368,340 subjects (median age, 58; men, 46.3%; median BCS, 11) were incorporated into the stroke and dementia outcome cohort, while 304,468 individuals were included in the late-life depression outcome cohort.

Over a median follow-up period of 12.5 years, 9361 stroke incidents, 6959 new dementia cases, and 14,371 new late-life depression cases were reported.

Every 5-point rise in BCS at baseline was independently linked to a reduced risk of 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).

Elevated genetic risk for stroke and diminished BCS were independently associated with a greater stroke risk. The independent HR for incident stroke was 73% (95% CI, 1.63-1.83) higher in individuals with high genetic risk compared to low genetic risk, while a 5-point increase in BCS led to a 30% (95% CI, 0.68-0.73) reduction.

In each genetic risk category, a higher BCS provided protection against stroke. For those with high genetic risk, the incident stroke rate was 1.2 per 1000 person-years among individuals with high BCS, compared to 2.8 per 1000 person-years for those with low BCS. In contrast, for individuals with low genetic risk, the incident stroke rates were 1.6 and 0.68 per 1000 person-years for those with high and low BCS, respectively.

Regarding late-life depression, increasing the BCS by 5 points was linked to a 35% (95% CI, 0.63-0.67) lower risk of this outcome, regardless of genetic predisposition. A high BCS corresponded to a 54% lower risk for late-life depression in participants with both high (HR, 0.46; 95% CI, 0.42-0.51) and low (HR, 0.46; 95% CI, 0.41-0.52) genetic susceptibility.

For individuals at high genetic risk, the incidence of late-life depression was 4.46 per 1000 person-years for those possessing a high BCS compared to 7.34 per 1000 person-years among those with low BCS. Standardized incidence rates among participants at low genetic risk were 3.17 and 4.58 per 1000 person-years for those with high and low BCS, respectively.

A 5-point disparity in BCS was correlated with an 18% reduced risk of dementia, independently 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 identified.

Among those with a heightened genetic risk for dementia, the incidence was 2.05 per 1000 person-years for individuals with high BCS and 3.64 per 1000 person-years for those with a low BCS.

The limitations of the study encompass the observational nature of the UK Biobank study, possible selection bias, and limited applicability of findings to a more diverse population.

“Additional studies are essential to prospectively explore the functionality and efficiency of the BCS as a targeted strategy in populations at increased genetic risk of age-related brain illnesses,” concluded the researchers.

Disclosure: One author has disclosed affiliations with biotech, pharmaceutical, and/or device companies. Please refer to the original publication for a comprehensive listing of authors’ disclosures.