scholarly journals Cerebral Glucose Metabolism as a Function of Age in Man: Influence of the Rate Constants in the Fluorodeoxyglucose Method

1983 ◽  
Vol 3 (2) ◽  
pp. 250-253 ◽  
Author(s):  
Randall A. Hawkins ◽  
John C. Mazziotta ◽  
Michael E. Phelps ◽  
Sung-Cheng Huang ◽  
David E. Kuhl ◽  
...  

Measurement of the local cerebral metabolic rate of glucose (LCMRGlc) with the fluorodeoxyglucose (FDG) method requires the utilization of appropriate values for the rate constants of the transport and phosphorylation processes. We measured these rate constants as a function of age to determine whether a decline in LCMRGlc as a function of age, in prior studies with the FDG method, actually represents changes in the rate constants. We found that measurements of LCMRGlc are not significantly affected by changes in rate constants as a function of aging, and that LCMRGlc did not change significantly with age.

1981 ◽  
Vol 1 (1) ◽  
pp. 37-51 ◽  
Author(s):  
Randall A. Hawkins ◽  
Michael E. Phelps> ◽  
Sung-Cheng Huang ◽  
David E. Kuhl

The model for quantifying local cerebral glucose metabolic rates originally developed by Sokoloff et al. and modified by Phelps, Huang and co-workers was applied to humans with cerebral ischemia (i.e., stroke). Rate constants for fluorodeoxyglucose were measured in ischemic and nonischemic regions with positron computed tomography. Using measured rate constants for ischemia, the model generates more accurate estimates of local cerebral glucose metabolism as compared to the use of rate constants from normal young adults, because the local metabolic rate is significantly underestimated, and temporal instability of the model is observed when normal values are applied to ischemic regions. A method was also developed to test the stability of the local lumped constant. The estimates of the lumped constant showed no or only small variations between ischemic and nonischemic types. Thus, errors introduced in the calculated local cerebral glucose metabolism by inappropriate rate constants appear to be more significant than those caused by any potential change in the lumped constant in ischemia.


1981 ◽  
Vol 1 (4) ◽  
pp. 391-401 ◽  
Author(s):  
Sung-Cheng Huang ◽  
Michael E. Phelps ◽  
Edward J. Hoffman ◽  
David E. Kuhl

The fluorodeoxyglucose (FDG) method for the measurement of local cerebral metabolic rate of glucose (LCMRGlc) employs typical values of the FDG transport rate constants that have been obtained by kinetic measurements on an appropriate control group. Discrepancies between the true values of the rate constants in tissue and the typical values used in the operational equation of the FDG method will introduce error in the estimate of LCMRGlc. Computer simulations were used to evaluate the accuracy of the FDG method in cases where (1) the tissue LCMRGlc deviates greatly from the normal values (e.g., stroke) or (2) the tissue LCMRGlc changes during the experiment (e.g., epileptic seizure). The effects of the magnitude and duration of metabolic changes were studied. The rsults indicate that if tissue LCMRGlc differs greatly from the normal value, the error in the estimated LCMRGlc at a scan time of 60 min is less than 20% of the difference between the true and normal values. In the non-steady-state cases, the estimated LCMRGlc was found to be a weighted average of the metabolic rates during the experiments, with the weightings approximately proportional to the plasma FDG concentration at the corresponding times. For example, if LCMRGlc in tissue was 5 times the normal values for the first 10 min but then returned to normal state, the LCMRGlc measured by the FDG method at a scan time of 60 min would be about only 2–3 times the normal value. The results of this study provide a better understanding of the accuracy of the FDG method under various tissue metabolic conditions and is useful for interpreting metabolic values obtained with the FDG method.


2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S670-S670
Author(s):  
Katsufumi Kajimoto ◽  
Naohiko Oku ◽  
Yasuyuki Kimura ◽  
Makiko Tanaka ◽  
Hiroki Kato ◽  
...  

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Julien Delrieu ◽  
Thierry Voisin ◽  
Laure Saint-Aubert ◽  
Isabelle Carrie ◽  
Christelle Cantet ◽  
...  

Abstract Background The Multidomain Alzheimer Preventive Trial (MAPT) was designed to assess the efficacy of omega-3 fatty acid supplementation, multidomain intervention (MI), or a combination of both on cognition. Although the MAPT study was negative, an effect of MI in maintaining cognitive functions compared to placebo group was showed in positive amyloid subjects. A FDG PET study (MAPT-NI) was implemented to test the impact of MI on brain glucose metabolism. Methods MAPT-NI was a randomized, controlled parallel-group single-center study, exploring the effect of MI on brain glucose metabolism. Participants were non-demented and had memory complaints, limitation in one instrumental activity of daily living, or slow gait. Participants were randomly assigned (1:1) to “MI group” or “No MI group.” The MI consisted of group sessions focusing on 3 domains: cognitive stimulation, physical activity, nutrition, and a preventive consultation. [18F]FDG PET scans were performed at baseline, 6 months, and 12 months, and cerebral magnetic resonance imaging scans at baseline. The primary objective was to evaluate the MI effect on brain glucose metabolism assessed by [18F]FDG PET imaging at 6 months. The primary outcome was the quantification of regional metabolism rate for glucose in cerebral regions involved early in Alzheimer disease by relative semi-quantitative SUVr (FDG-based AD biomarker). An exploratory voxel-wise analysis was performed to assess the effect of MI on brain glucose metabolism without anatomical hypothesis. Results The intention-to-treat population included 67 subjects (34 in the MI group and 33 in the No MI group. No significant MI effect was observed on primary outcome at 6 months. In the exploratory voxel-wise analysis, we observed a difference in favor of MI group on the change of cerebral glucose metabolism in limbic lobe (right hippocampus, right posterior cingulate, left posterior parahippocampal gyrus) at 6 months. Conclusions MI failed to show an effect on metabolism in FDG-based AD biomarker, but exploratory analysis suggested positive effect on limbic system metabolism. This finding could suggest a delay effect of MI on AD progression. Trial registration ClinicalTrials.gov Identifier, NCT01513252.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yo-Han Joo ◽  
Yun-Kwan Kim ◽  
In-Gyu Choi ◽  
Hyeon-Jin Kim ◽  
Young-Don Son ◽  
...  

Abstract Background Perturbed functional coupling between the metabotropic glutamate receptor-5 (mGluR5) and N-methyl-d-aspartate (NMDA) receptor-mediated excitatory glutamatergic neurotransmission may contribute to the pathophysiology of psychiatric disorders such as schizophrenia. We aimed to establish the functional interaction between mGluR5 and NMDA receptors in brain of mice with genetic ablation of the mGluR5. Methods We first measured the brain glutamate levels with magnetic resonance spectroscopy (MRS) in mGluR5 knockout (KO) and wild-type (WT) mice. Then, we assessed brain glucose metabolism with [18F]fluorodeoxyglucose ([18F]FDG) positron emission tomography before and after the acute administration of an NMDA antagonist, MK-801 (0.5 mg/kg), in the same mGluR5 KO and WT mice. Results Between-group comparisons showed no significant differences in [18F]FDG standardized uptake values (SUVs) in brain of mGluR5 KO and WT mice at baseline, but widespread reductions in mGluR5 KO mice compared to WT mice after MK-801 administration (p < 0.05). The baseline glutamate levels did not differ significantly between the two groups. However, there were significant negative correlations between baseline prefrontal glutamate levels and regional [18F]FDG SUVs in mGluR5 KO mice (p < 0.05), but no such correlations in WT mice. Fisher’s Z-transformation analysis revealed significant between-group differences in these correlations (p < 0.05). Conclusions This is the first multimodal neuroimaging study in mGluR5 KO mice and the first report on the association between cerebral glucose metabolism and glutamate levels in living rodents. The results indicate that mGluR5 KO mice respond to NMDA antagonism with reduced cerebral glucose metabolism, suggesting that mGluR5 transmission normally moderates the net effects of NMDA receptor antagonism on neuronal activity. The negative correlation between glutamate levels and glucose metabolism in mGluR5 KO mice at baseline may suggest an unmasking of an inhibitory component of the glutamatergic regulation of neuronal energy metabolism.


2015 ◽  
Vol 6 ◽  
Author(s):  
Hibah O. Awwad ◽  
Larry P. Gonzalez ◽  
Paul Tompkins ◽  
Megan Lerner ◽  
Daniel J. Brackett ◽  
...  

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