La Hood Alexandra, Moran Chris, Than Stephanie, Lu Alicia, Collyer Taya A, Beare Richard, Srikanth Velandai
Peninsula Clinical School, School of Translational Medicine, Monash University, PO Box 52, Frankston, VIC, 3199, Australia.
Department of Geriatric Medicine, Peninsula Health, 24 Separation Street, Mornington, VIC, 3931, Australia.
Sci Rep. 2025 May 29;15(1):18896. doi: 10.1038/s41598-025-04010-7.
Low physical activity (PA) and obesity are dementia risk factors, but it is unclear whether the association between PA and brain health is dependent upon degree of obesity. We aimed to examine the association between PA and brain structure and explore whether it varies by body mass index (BMI). We examined the associations between accelerometer-measured PA and magnetic resonance imaging-measured brain structure using cross-sectional data from a population-based cohort of people in midlife (UK Biobank). Using regression modelling, we explored whether these associations were mediated by BMI or other cardiometabolic risk factors. Complete data were available for 16,725 participants (median age 65 years, 55% women, median BMI 26). Greater PA was positively associated with total brain (β = 3.67, p < 0.0001), grey matter (β = 3.12, p < 0.0001), white matter (β = 0.43, p < 0.0001) and total hippocampal volumes (β = 0.05, p < 0.0001), and inversely associated with white matter hyperintensity volume (β = - 4.6 × 10, p < 0.0001). Although there was no interaction between PA and BMI in explaining brain volumes, BMI attenuated the PA-brain volume associations by between 18 and 58%. The PA-brain volume associations were further attenuated by other cardiometabolic risk factors and in the case of grey matter and hippocampal volume, was no longer statistically significant in fully adjusted models. Greater PA is associated with a healthier profile in brain volumes. BMI and cardiometabolic factors mediated the relationship between PA and grey matter and hippocampal volume and partially mediated its relationship with other brain volumes. These results support a mechanistic basis for PA in optimizing cardiometabolic risk for dementia prevention.
低体力活动（PA）和肥胖是痴呆症的风险因素，但尚不清楚PA与大脑健康之间的关联是否取决于肥胖程度。我们旨在研究PA与脑结构之间的关联，并探讨其是否因体重指数（BMI）而异。我们使用来自一个基于人群的中年队列（英国生物银行）的横断面数据，研究了加速度计测量的PA与磁共振成像测量的脑结构之间的关联。通过回归模型，我们探讨了这些关联是否由BMI或其他心血管代谢风险因素介导。共有16725名参与者（中位年龄65岁，55%为女性，中位BMI为26）获得了完整数据。较高的PA与全脑体积（β = 3.67，p < 0.0001）、灰质体积（β = 3.12，p < 0.0001）、白质体积（β = 0.43，p < 0.0001）和海马总体积（β = 0.05，p < 0.0001）呈正相关，与白质高信号体积呈负相关（β = -4.6×10，p < 0.0001）。虽然在解释脑体积方面PA和BMI之间没有相互作用，但BMI使PA与脑体积之间的关联减弱了18%至58%。PA与脑体积之间的关联进一步被其他心血管代谢风险因素减弱，对于灰质和海马体积而言，在完全调整模型中不再具有统计学意义。较高的PA与更健康的脑体积特征相关。BMI和心血管代谢因素介导了PA与灰质和海马体积之间的关系，并部分介导了其与其他脑体积之间的关系。这些结果为PA在优化心血管代谢风险以预防痴呆症方面提供了一个机制基础。
