Publication Type	Academic Article
Authors	Shin J, Tsui W, Li Y, Lee S, Kim S, Cho S, Kim Y, de Leon M
Journal	Int J Alzheimers Dis
Volume	2011
Pagination	759780
Date Published	03/17/2011
ISSN	2090-0252
Abstract	It has been suggested that glucose metabolism within the brain's default network is directly associated with-and may even cause-the amyloid pathology of Alzheimer's disease (AD). Here we performed 2-[(18)F]fluoro-2-deoxy-D-glucose (FDG) and [(11)C]-labeled Pittsburgh Compound B (PIB) positron emission tomography (PET) on cognitively normal elderly subjects and on AD patients and conducted quantitative regional analysis of FDG- and PIB-PET images using an automated region of interest technique. We confirmed that resting glucose metabolism within the posterior components of the brain's default network is high in normal elderly subjects and low in AD patients, which is partially in agreement with the regional pattern of PIB uptake within the default network of AD patients. However, in several regions outside the default network, glucose metabolism was high in normal elderly subjects but was not depressed in AD patients, who exhibited significantly increased PIB uptakes in these regions. In contrast, the level of resting glucose metabolism in the default network and in regions outside the default network in normal elderly subjects was significantly correlated with the level of regional PIB uptake in AD patients. These results are discussed with experimental evidence suggesting that beta amyloid production and amyloid precursor protein regulation are dependent on neuronal activity.
DOI	10.4061/2011/759780
PubMed ID	21461406
PubMed Central ID	PMC3065040