The aim of the study was to investigate the relationships between cerebrospinal fluid (CSF) levels of t-Tau, p-Tau and amyloid-β (Aβ1–42) amyloid peptide and fluorine-18 fluorodeoxyglucose (18F-FDG) brain distribution in a group of patients with Alzheimer’s disease.
Materials and methods
The study included 81 newly diagnosed Alzheimer’s disease patients according to the NINCDS-ADRDA criteria. The mean (±SD) age of the patients was 70 (±6) years; 44 were male and 37 were female. All patients underwent a CSF assay and MRI before 18F-FDG PET scanning. The relationships were evaluated by means of statistical parametric mapping (SPM8).
Increased t-Tau CSF levels were related to reduced glucose consumption in a wide portion of the right frontal lobe [Brodmann area (BA 47)] and limbic lobe bilaterally (BA 31,32), whereas no areas of increased 18F-FDG uptake related to t-Tau levels were detected. Elevated p-Tau concentrations in CSF were related to increased glucose consumption in both the right and the left limbic lobe and in the left frontal lobe (BA 32 and 8). We did not find any specific cortical area of reduced glucose consumption being related to low levels of Aβ1–42 in CSF, whereas a spawn of 18F-FDG uptake was detectable in BA 18,19 and in the right cerebellum.
The results of our study suggest that reduced Aβ1–42 concentrations in CSF are related to a wide cortical dysfunction, whereas t-Tau and p-Tau are related to more selective cortical metabolic patterns that mainly involve the cingulate cortex.