Lack of association between cortical amyloid deposition and glucose metabolism in early stage Alzheimer ' s disease patients

Background Beta amyloid (A beta) causes synaptic dysfunction leading to neuronal death. It is still controversial if the magnitude of A beta deposition correlates with the degree of cognitive impairment. Diagnostic imaging may lead to a better understanding the role of A beta in development of cognitive deficits. The aim of the present study was to investigate if A beta deposition in the corresponding brain region of early stage Alzheimer ' s disease (AD) patients, directly correlates to neuronal dysfunction and cognitive impairment indicated by reduced glucose metabolism. Patients and methods In 30 patients with a clinical phenotype of AD and amyloid positive brain imaging, 2-[18F] fluoro-2-deoxy-d-glucose (FDG) PET/CT was performed. We extracted the average [18F] flutemetamol (Vizamyl) uptake for each of the 16 regions of interest in both hemispheres and computed the standardized uptake value ratio (SUVR) by dividing the Vimazyl intensities by the mean signal of positive and negative control regions. Data were analysed using the R environment for statistical computing and graphics. Results Any negative correlation between A beta deposition and glucose metabolism in 32 dementia related and corresponding brain regions in AD patients was not found. None of the correlation coefficient values were statistically significant different from zero based on two-sided p- value. Conclusions Regional A beta deposition did not correlate negatively with local glucose metabolism in early stage AD patients. Our findings support the role of A beta as a valid biomarker, but does not permit to conclude that A beta is a direct cause for an aberrant brain glucose metabolism and neuronal dysfunction.