阿尔茨海默症患者灰质萎缩与认知评分具有相关性:基于体素的形态学测量方法OA

Objective To investigate regional alterations in gray matter volume(GMV)among patients with Alzheimer's disease(AD)using voxel-based morphometry(VBM),and to explore the association between these structural changes and clinical cognitive assessment scores.Methods A total of 61 participants were selected from the Alzheimer's Disease Neuroimaging Initiative database.Based on predefined inclusion and exclusion criteria,subjects were categorized into two groups:32 individuals diagnosed with AD(AD group)and 29 cognitively healthy controls(HC group).VBM was applied to calculate and compare GMV across groups.Significant intergroup differences in brain regions were identified using a dual-threshold statistical approach involving voxel-level family-wise error(FWE)correction and cluster-level false discovery rate(FDR)correction(P<0.05).Brain regions exhibiting significant atrophy were further analyzed for correlations with clinical scale scores,specifically,the Mini-Mental State Examination(MMSE)and Clinical Dementia Rating(CDR),using Pearson correlation analysis.Results Total GMV was significantly reduced in the AD group compared to the HC group(P<0.05).Regional analyses revealed three clusters showing significant GMV reductions in AD patients,with peak coordinates located in the right superior temporal pole,left amygdala,and left middle cingulate gyrus.As anticipated,the AD group performed significantly worse on both MMSE and CDR assessments(P<0.001).Correlation analyses demonstrated that,within the AD group,higher MMSE scores were positively associated with GMV in all three affected regions(P<0.05).In contrast,CDR scores showed negative correlations with GMV in the right superior temporal pole and left amygdala(P<0.05).Conclusion VBM analysis confirms characteristic patterns of gray matter atrophy in AD,predominantly affecting the temporal pole,amygdala,and cingulate cortex.The significant associations between regional GMV loss and cognitive performance suggest that such structural changes may represent key neuroanatomical substrates underlying the clinical symptoms and pathophysiological progression of AD.