PURPOSE: Our aim was to study the correlations between cerebrospinal fluid (CSF) biomarker levels such as beta-amyloid 42 (Abeta(42)), total and phosphorylated tau protein (T-tau and P-tau) and brain perfusion SPECT in Alzheimer's disease (AD) using a voxel-based methodology. METHODS: Patients (n = 31) with clinical features of AD (n = 25) or amnestic mild cognitive impairment (aMCI) (n = 6) were retrospectively included. All subjects underwent the same clinical, neuropsychological and neuroimaging tests. They had a lumbar puncture and a brain perfusion ((99m)Tc-ECD) SPECT within a time interval of 10 (+/-26) days. Correlations between CSF biomarker concentrations and perfusion were studied using SPM2 software. Individual normalised regional activity values were extracted from the eligible clusters for calculation of correlation coefficients. RESULTS: No significant correlation was found between Abeta(42) concentrations and brain perfusion. A significant correlation (p < 0.01, corrected) was found between T-tau or P-tau concentrations and perfusion in the left parietal cortex. CONCLUSION: Our results suggest a strong correlation between T-tau and P-tau levels and decreased brain perfusion in regions typically affected by neuropathological changes in AD.
PURPOSE: Our aim was to study the correlations between cerebrospinal fluid (CSF) biomarker levels such as beta-amyloid 42 (Abeta(42)), total and phosphorylated tau protein (T-tau and P-tau) and brain perfusion SPECT in Alzheimer's disease (AD) using a voxel-based methodology. METHODS:Patients (n = 31) with clinical features of AD (n = 25) or amnestic mild cognitive impairment (aMCI) (n = 6) were retrospectively included. All subjects underwent the same clinical, neuropsychological and neuroimaging tests. They had a lumbar puncture and a brain perfusion ((99m)Tc-ECD) SPECT within a time interval of 10 (+/-26) days. Correlations between CSF biomarker concentrations and perfusion were studied using SPM2 software. Individual normalised regional activity values were extracted from the eligible clusters for calculation of correlation coefficients. RESULTS: No significant correlation was found between Abeta(42) concentrations and brain perfusion. A significant correlation (p < 0.01, corrected) was found between T-tau or P-tau concentrations and perfusion in the left parietal cortex. CONCLUSION: Our results suggest a strong correlation between T-tau and P-tau levels and decreased brain perfusion in regions typically affected by neuropathological changes in AD.
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