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O4‐09‐02: Diagnostic value of molecular imaging in a memory clinic setting
Author(s) -
Ossenkoppele Rik,
Prins Niels,
Pijnenburg Yolande,
Lemstra Evelien,
Van der Flier Wiesje,
Windhorst Albert,
Hoekstra Otto,
Lammertsma Adriaan,
Scheltens Philip,
Berckel Bart
Publication year - 2012
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2012.05.1684
Subject(s) - dementia with lewy bodies , memory clinic , medicine , dementia , frontotemporal dementia , medical diagnosis , memory impairment , population , confidence interval , clinical dementia rating , standardized uptake value , disease , nuclear medicine , positron emission tomography , radiology , psychiatry , cognition , environmental health
whether PiB retention between baseline and 24-months increased (PiB-increase) or was stable (PiB-stable). Results: 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. Conclusions: 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 Ab-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, Ab did not directly caused reactive hypermetabolism in MCI, suggesting that higher basal metabolism (i.e., higher brain reserve) was increasing the level of Ab 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.