Frontiers in aging neuroscience · 2026
From muscle to brain: the mediating effect of vitamin D in the relationship between muscle loss and cognitive function in Alzheimer's disease.
СтатьяНазвание и аннотация: Перевод в очереди
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Ma Xiaoting, Yao Linlin, Li Fangbo, Cui Chong, Wang Erlei, Wang Caishan, Zhao Ping, Weng Xiaofen, Liu Chunfeng, Liu Shanwen, Hu Hua
Аннотация
OBJECTIVE: To investigate the association among Vitamin D (VD), muscle loss and cognitive function, and further analyze the possible role of VD in the association between muscle loss and cognitive function in patients with Alzheimer's disease (AD).
METHODS: This cross-sectional study included 58 patients with AD (30 mild and 28 moderate) and 30 neurotypical controls (NC). Demographic data, neuropsychological tests, and serum VD levels were collected. Muscle loss related indicators, including both clinical macroscopic and morphological microstructural indicators, were measured.
RESULTS: The differences among 3 groups in different cognitive domains, muscle loss related indicators and serum VD levels were statistically significant (P < 0.05). Adjusted for age, sex and BMI, correlations were observed among broad cognitive domains, muscle loss related indicators (especially muscle mass and upper limb muscle strength) and serum VD levels in patients with AD (P < 0.05). Mediation analyses revealed that muscle loss, particularly muscle mass reduction, significantly impacted cognitive function in patients with AD (P < 0.05). This effect remained statistically significant after accounting for VD levels (P < 0.05), and VD deficiency partially mediated the effect of muscle loss on cognitive function (P < 0.05).
CONCLUSION: VD level, muscle loss, and cognitive dysfunction are closely related, and VD partially mediated the association between muscle mass reduction and cognitive dysfunction in patients with AD. These preliminary findings highlight the importance of assessing muscle loss and VD deficiency, and suggest that targeted intervention may be a valuable management strategy for the AD population.
METHODS: This cross-sectional study included 58 patients with AD (30 mild and 28 moderate) and 30 neurotypical controls (NC). Demographic data, neuropsychological tests, and serum VD levels were collected. Muscle loss related indicators, including both clinical macroscopic and morphological microstructural indicators, were measured.
RESULTS: The differences among 3 groups in different cognitive domains, muscle loss related indicators and serum VD levels were statistically significant (P < 0.05). Adjusted for age, sex and BMI, correlations were observed among broad cognitive domains, muscle loss related indicators (especially muscle mass and upper limb muscle strength) and serum VD levels in patients with AD (P < 0.05). Mediation analyses revealed that muscle loss, particularly muscle mass reduction, significantly impacted cognitive function in patients with AD (P < 0.05). This effect remained statistically significant after accounting for VD levels (P < 0.05), and VD deficiency partially mediated the effect of muscle loss on cognitive function (P < 0.05).
CONCLUSION: VD level, muscle loss, and cognitive dysfunction are closely related, and VD partially mediated the association between muscle mass reduction and cognitive dysfunction in patients with AD. These preliminary findings highlight the importance of assessing muscle loss and VD deficiency, and suggest that targeted intervention may be a valuable management strategy for the AD population.