Clinical imaging · 2026
Liver steatosis and cognitive performance in aging: A pilot cross-sectional study.
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Khalafi Mohammad, Hojjati Seyed Hani, Wang Xiuyuan Hugh, Tanzi Emily B, Liao Vanessa, Kumar Sonal, Parikh Neal S, Chiang Gloria C
Аннотация
PURPOSE: Metabolic dysfunction-associated steatotic liver disease (MASLD) has been linked to dementia. We investigated whether liver steatosis or fibrosis is associated with early cognitive changes, while exploring related mechanisms like body mass index (BMI) and cerebral β-amyloid deposition.
METHODS: In this cross-sectional study, we enrolled 26 cognitively unimpaired individuals, who underwent amyloid PET and comprehensive clinical, neurological, and neuropsychological evaluations, including the Telephone Interview for Cognitive Status (TICS). Liver steatosis and fibrosis were quantified noninvasively using vibration-controlled transient elastography (FibroScan®; Echosens, Paris, France) with an M-probe, with the controlled attenuation parameter (CAP) used to quantify liver steatosis. Multivariate regression models were used to assess relationships between liver and cognitive measures, adjusting for age.
RESULTS: In our cohort (mean age 72.2 ± 8.4 years), greater liver steatosis was associated with lower TICS scores, using both the CAP score (β = -0.03, p = 0.021) and steatosis grade (β = -1.39, p = 0.023). Higher liver stiffness was also negatively associated with TICS scores (β = -1.39, p = 0.042). BMI was significantly associated with greater cerebral amyloid burden (β = 9.03, p = 0.01), higher steatosis grade (β = 0.30, p = 0.03), and higher CAP scores (β = 9.47, p = 0.003).
CONCLUSION: Liver steatosis associates with lower cognitive scores in older adults. BMI associates with both steatosis and amyloid burden, which may reflect co-occurring metabolic pathways. These findings provide evidence for targeting metabolic health to preserve cognition and mitigate Alzheimer's pathology.
METHODS: In this cross-sectional study, we enrolled 26 cognitively unimpaired individuals, who underwent amyloid PET and comprehensive clinical, neurological, and neuropsychological evaluations, including the Telephone Interview for Cognitive Status (TICS). Liver steatosis and fibrosis were quantified noninvasively using vibration-controlled transient elastography (FibroScan®; Echosens, Paris, France) with an M-probe, with the controlled attenuation parameter (CAP) used to quantify liver steatosis. Multivariate regression models were used to assess relationships between liver and cognitive measures, adjusting for age.
RESULTS: In our cohort (mean age 72.2 ± 8.4 years), greater liver steatosis was associated with lower TICS scores, using both the CAP score (β = -0.03, p = 0.021) and steatosis grade (β = -1.39, p = 0.023). Higher liver stiffness was also negatively associated with TICS scores (β = -1.39, p = 0.042). BMI was significantly associated with greater cerebral amyloid burden (β = 9.03, p = 0.01), higher steatosis grade (β = 0.30, p = 0.03), and higher CAP scores (β = 9.47, p = 0.003).
CONCLUSION: Liver steatosis associates with lower cognitive scores in older adults. BMI associates with both steatosis and amyloid burden, which may reflect co-occurring metabolic pathways. These findings provide evidence for targeting metabolic health to preserve cognition and mitigate Alzheimer's pathology.