IC‐02‐03: Hypometabolism of the posterior cingulate cortex is not restricted to Alzheimer's disease

Posterior cingulate Statistical parametric mapping Pathophysiology Amyloid (mycology)
DOI: 10.1016/j.jalz.2015.06.009 Publication Date: 2015-12-15T10:35:57Z
ABSTRACT
Hypometabolism of the posterior cingulate cortex (PCC) is associated with Alzheimer's disease (AD). PCC vulnerability, however, could also be present in other neurodegenerative diseases, such as behavioural variant frontotemporal dementia (bvFTD), and normal aging. The aims this study were to assess 1) proportion AD, bvFTD cognitive subjects (CN) hypometabolism, 2) relationship between metabolism demographical, neuropsychological, neurobiological characteristics CN. We included 33 probable patients (Neary criteria, low likelihood AD pathophysiology based on CSF amyloid-beta1-42 >550ng/l), 82 (National Institute Aging-Alzheimer's Association workgroups core high tau/amyloid-beta1-42 >.52ng/l), 26 CN (22 subjective memory complaints 4 healthy controls, >550ng/l). Glucose was assessed using [18F]FDG-PET. Parametric images standardized uptake value ratios (SUVr) cerebellar grey matter reference tissue generated. First, we defined hypometabolism Receiver Operating Characteristic (ROC) separating from CN, relative prevalence Second, explored relationships demographics (age, sex, education), Mini-Mental State Examination (MMSE), neuropsychological tests, biomarkers (amyloid-beta1-42, tau phosphorylated tau), APOE genotype within diagnostic groups linear regression analyses or ANOVA where appropriate. Mean age 63±7 (AD), 65±8 (bvFTD) 61±8 years old. [18F]FDG SUVr > AD. Based optimal discrimination cut-off set at 1.052, resulting 78% 33% 23% (CN). (beta±SE: -.007±.002, p=.002) -.007±.003, p=.011), not In context work-up dementia, it important realize that vulnerability restricted but
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