Regional Cerebral Glucose Metabolism in Healthy Volunteers Determined by Fluordeoxyglucose Positron Emission Tomography

Ivančević, Velimir; Alavi, A.; Souder, Elaine; Mozley, P. David; Gur, Raquel E.; Bénard, François; Munz, Dieter L.

doi:10.1097/00003072-200008000-00005

Cited by 28 publications

(20 citation statements)

References 13 publications

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“…The increases in the brain levels of Glc may be a sign of diminished Glc utilization which would be consistent with observations of reduced Glc metabolic rates in human brain during aging, especially in the frontal and temporal cortex [71, 72]. Such decreases in Glc metabolic rates may result from either cell damage or from shifts in the use of Lac in place of Glc as substrate for oxidative phosphorylation in hyper-activated neurons of the Tg mouse brains.…”

Section: Discussionsupporting

confidence: 86%

Metabolism Changes During Aging in the Hippocampus and Striatum of Glud1 (Glutamate Dehydrogenase 1) Transgenic Mice

et al. 2014

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The decline in neuronal function during aging may result from increases in extracellular glutamate (Glu), Glu-induced neurotoxicity, and altered mitochondrial metabolism. To study metabolic responses to persistently high levels of Glu at synapses during aging, we used transgenic (Tg) mice that over-express the enzyme Glu dehydrogenase (GDH) in brain neurons and release excess Glu in synapses. Mitochondrial GDH is important in amino acid and carbohydrate metabolism and in anaplerotic reactions. We monitored changes in nineteen neurochemicals in the hippocampus and striatum of adult, middle aged, and aged Tg and wild type (wt) mice, in vivo, using proton (1H) magnetic resonance spectroscopy. Significant differences between adult Tg and wt were higher Glu, N-acetyl aspartate (NAA), and NAA + NAA−Glu (NAAG) levels, and lower lactate in the Tg hippocampus and striatum than those of wt. During aging, consistent changes in Tg and wt hippocampus and striatum included increases in myo-inositol and NAAG. The levels of glutamine (Gln), a key neurochemical in the Gln-Glu cycle between neurons and astroglia, increased during aging in both the striatum and hippocampus of Tg mice, but only in the striatum of the wt mice. Age-related increases of Glu were observed only in the striatum of the Tg mice.

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Section: Discussionsupporting

confidence: 86%

Metabolism Changes During Aging in the Hippocampus and Striatum of Glud1 (Glutamate Dehydrogenase 1) Transgenic Mice

et al. 2014

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“…The posterior cingulate has the highest rate of glucose metabolism at rest of any cortical region (Ivancevic et al, 2000), perhaps because of its role as one of the major hubs of the default mode network (Buckner et al, 2008). One of the principles of posterior cingulate physiology is that it tends to be tonically active (Raichle et al, 2001) but deactivates when mental effort is required.…”

Section: Discussionmentioning

confidence: 99%

18F-fluorodeoxyglucose positron emission tomography, aging, and apolipoprotein E genotype in cognitively normal persons

Knopman

Jack

Wiste

et al. 2014

Neurobiology of Aging

106

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Our objective was to examine associations between glucose metabolism, as measured by 18F-fluorodeoxyglucose positron emission tomography (FDG PET), and age and to evaluate the impact of carriage of an apolipoprotein E (APOE) ε4 allele on glucose metabolism and on the associations between glucose metabolism and age. We studied 806 cognitively normal (CN) and 70 amyloid-imaging-positive cognitively impaired participants (35 with mild cognitive impairment and 35 with Alzheimer’s disease [AD] dementia) from the Mayo Clinic Study of Aging, Mayo Alzheimer’s Disease Research Center and an ancillary study who had undergone structural MRI, FDG PET, and 11C-Pittsburgh compound B (PiB) PET. Using partial volume corrected and uncorrected FDG PET glucose uptake ratios, we evaluated associations of regional FDG ratios with age and carriage of an APOE ε4 allele in CN participants between the ages of 30 and 95 years, and compared those findings with the cognitively impaired participants. In region-of-interest (ROI) analyses, we found modest but statistically significant declines in FDG ratio in most cortical and subcortical regions as a function of age. We also found a main effect of APOE ε4 genotype on FDG ratio, with greater uptake in ε4 noncarriers compared with carriers but only in the posterior cingulate and/or precuneus, lateral parietal, and AD-signature meta-ROI. The latter consisted of voxels from posterior cingulate and/or precuneus, lateral parietal, and inferior temporal. In age- and sex-matched CN participants the magnitude of the difference in partial volume corrected FDG ratio in the AD-signature meta-ROI for APOE ε4 carriers compared with noncarriers was about 4 times smaller than the magnitude of the difference between age- and sex-matched elderly APOE ε4 carrier CN compared with AD dementia participants. In an analysis in participants older than 70 years (31.3% of whom had elevated PiB), there was no interaction between PiB status and APOE ε4 genotype with respect to glucose metabolism. Glucose metabolism declines with age in many brain regions. Carriage of an APOE ε4 allele was associated with reductions in FDG ratio in the posterior cingulate and/or precuneus, lateral parietal, and AD-signature ROIs, and there was no interaction between age and APOE ε4 status. The posterior cingulate and/or precuneus and lateral parietal regions have a unique vulnerability to reductions in glucose metabolic rate as a function both of age and carriage of an APOE ε4 allele.

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“…The majority of the brain glucose is converted to ATP energy for the maintenance of normal neuronal functions including cognition. In AD reduction of the brain glucose utilization differs regionally [124,144–146]. According to Hoyer [147] this variation is a cause for neurodegeneration rather than a mere consequence.…”

Section: Alzheimer’s Disease: Glucose Metabolism and Glucose Transmentioning

confidence: 99%

The Role of Glucose Transporters in Brain Disease: Diabetes and Alzheimer’s Disease

Shah

Silva

Abbruscato

2012

IJMS

231

175

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The occurrence of altered brain glucose metabolism has long been suggested in both diabetes and Alzheimer’s diseases. However, the preceding mechanism to altered glucose metabolism has not been well understood. Glucose enters the brain via glucose transporters primarily present at the blood-brain barrier. Any changes in glucose transporter function and expression dramatically affects brain glucose homeostasis and function. In the brains of both diabetic and Alzheimer’s disease patients, changes in glucose transporter function and expression have been observed, but a possible link between the altered glucose transporter function and disease progress is missing. Future recognition of the role of new glucose transporter isoforms in the brain may provide a better understanding of brain glucose metabolism in normal and disease states. Elucidation of clinical pathological mechanisms related to glucose transport and metabolism may provide common links to the etiology of these two diseases. Considering these facts, in this review we provide a current understanding of the vital roles of a variety of glucose transporters in the normal, diabetic and Alzheimer’s disease brain.

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Regional Cerebral Glucose Metabolism in Healthy Volunteers Determined by Fluordeoxyglucose Positron Emission Tomography

Abstract: All three projection planes must be used for a comprehensive qualitative evaluation of the regional glucose metabolism of the brain.

Cited by 28 publications

References 13 publications

Metabolism Changes During Aging in the Hippocampus and Striatum of Glud1 (Glutamate Dehydrogenase 1) Transgenic Mice

Metabolism Changes During Aging in the Hippocampus and Striatum of Glud1 (Glutamate Dehydrogenase 1) Transgenic Mice

18F-fluorodeoxyglucose positron emission tomography, aging, and apolipoprotein E genotype in cognitively normal persons

The Role of Glucose Transporters in Brain Disease: Diabetes and Alzheimer’s Disease

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