O4‐09‐01: Increases in Pittsburgh compound B retention are associated with increased cerebral glucose metabolism in cognitively normal elderly: Role for compensatory hypermetabolism?
Year: 2012
Type: article
Study design: Observational Study
Abstract: Inverse correlations between Aβ measured by PiB-PET and cerebral metabolism using FDG-PET in Alzheimer's disease (AD) suggests local Aβ-induced metabolic insults at this stage of cognitive impairment. We previously explored PiB and FDG relationships in MCI (Cohen et al., 2009). In the current study, we explored FDG metabolism in cognitively normal elderly subjects (NC) with and without increased PiB-retention over a 24-months. PiB PET and FDG PET was performed in 50 NC (80±6 years; MMSE: 28±2; 70% female) at baseline and 24-months. Tissue ratios were calculated for cortical regions-of-interest for both tracers, using cerebellum as reference (SUVR). Subjects were divided by cluster analysis into two groups depending on whether PiB retention between baseline and 24-months increased (PiB-increase) or was stable (PiB-stable). At baseline, there were no significant differences in FDG or PiB SUVR between groups. However, the PiB-increase group showed significant increases in FDG metabolism in both anterior cingulate and frontal cortices from baseline to 24-month when compared to the PiB-stable group (P>0.01). In addition, the PiB-increase group showed significantly higher FDG-SUVR values in anterior cingulate and frontal cortices at 24 months compared to PiB-stable subjects (P>0.05). Neither of these finding were apparent when subjects were split only by PiB(+) and PiB(-) status rather than by PiB-stable vs. PiB-increase status. NC subjects with increased PiB show an increase in FDG over a 24-month period in frontal cortical regions compared to subjects with stable PiB. These data suggest that a reactive hypermetabolism occurs in NC subjects as Aβ-load increases in the brain. This phenomenon does not appear to persist as cognitive impairments appear, because in mild cognitive impairment (MCI), we have previously observed positive correlations between PiB and FDG, particularly in frontal brain regions, however, there was no corresponding increase in metabolism. Therefore, unlike the current observation in controls, Aβ did not directly caused reactive hypermetabolism in MCI, suggesting that higher basal metabolism (i.e., higher brain reserve) was increasing the level of Aβ necessary to cause conversion to dementia. These findings also suggest that additional information is present in the trajectory of PiB retention that is not available cross-sectionally.
Source: Alzheimer s & Dementia
Institution: University of Pittsburgh
Language: English
Subfield: Psychiatry and Mental health
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W2015503808