Frontiers in neurology · 2026
Gray matter atrophy mediates the association between cerebral hypometabolism and cognitive impairment in Alzheimer's disease.
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Zhao Shiqi, Chen Jianwen, Li Peixue, Zhao Li, Dong Chunbo, Yu Lei
Аннотация
OBJECTIVE: Alzheimer's disease (AD) is characterized by amyloid deposition, brain hypometabolism, gray matter atrophy and cognitive decline, yet their causal interactions are poorly defined. This multimodal PET/MRI study explored regional gray matter volume (GMV) loss and glucose hypometabolism in AD patients, and clarified their correlations with distinct cognitive deficits alongside mediating pathways.
METHODS: 134 probable dementia patients were split into AD and non-AD dementia cohorts based on 18F-AV45 PET amyloid-β (Aβ) load, all receiving structural MRI, 18F-FDG and 18F-AV45 PET scans. We compared intergroup GMV and metabolic discrepancies, analyzed imaging-cognition correlations adjusted for clinical and demographic confounders, and implemented mediation models to test whether GMV bridges cerebral metabolism and cognition.
RESULTS: AD patients exhibited prominent regional GMV shrinkage and FDG hypometabolism in vulnerable brain regions relative to non-AD dementia subjects. Covariate-adjusted analyses linked both imaging biomarkers to domain-specific cognitive performance. Primary mediation analyses showed that regional GMV significantly mediated the associations between FDG metabolism and visuospatial, executive, and language function, accounting for 40.36, 35.60, and 49.99% of the total effects, respectively. Reverse mediation models identified only a weak indirect effect of right superior temporal gyrus metabolism on the association between right inferior parietal lobule GMV and visuospatial ability, accounting for 13.26% of the total effect. Moreover, after multiple-imputation sensitivity analyses, most indirect effects became unstable or nonsignificant, suggesting that the FDG metabolism-cognition association is predominantly direct, with limited evidence for GMV mediation.
CONCLUSION: Integrated PET/MRI revealed AD-related patterns of regional atrophy and hypometabolism. Overall, the association between cerebral metabolic dysfunction and cognitive impairment appeared to be predominantly direct, with limited evidence supporting a mediating role of regional GMV.
METHODS: 134 probable dementia patients were split into AD and non-AD dementia cohorts based on 18F-AV45 PET amyloid-β (Aβ) load, all receiving structural MRI, 18F-FDG and 18F-AV45 PET scans. We compared intergroup GMV and metabolic discrepancies, analyzed imaging-cognition correlations adjusted for clinical and demographic confounders, and implemented mediation models to test whether GMV bridges cerebral metabolism and cognition.
RESULTS: AD patients exhibited prominent regional GMV shrinkage and FDG hypometabolism in vulnerable brain regions relative to non-AD dementia subjects. Covariate-adjusted analyses linked both imaging biomarkers to domain-specific cognitive performance. Primary mediation analyses showed that regional GMV significantly mediated the associations between FDG metabolism and visuospatial, executive, and language function, accounting for 40.36, 35.60, and 49.99% of the total effects, respectively. Reverse mediation models identified only a weak indirect effect of right superior temporal gyrus metabolism on the association between right inferior parietal lobule GMV and visuospatial ability, accounting for 13.26% of the total effect. Moreover, after multiple-imputation sensitivity analyses, most indirect effects became unstable or nonsignificant, suggesting that the FDG metabolism-cognition association is predominantly direct, with limited evidence for GMV mediation.
CONCLUSION: Integrated PET/MRI revealed AD-related patterns of regional atrophy and hypometabolism. Overall, the association between cerebral metabolic dysfunction and cognitive impairment appeared to be predominantly direct, with limited evidence supporting a mediating role of regional GMV.