Diminished glucose transport in alzheimer's disease: Dynamic PET studies

William J. Jagust, J. Philip Seab, Ronald H. Huesman, Peter E. Valk, Chester A. Mathis, Bruce R Reed, Pamela G. Coxson, Thomas F. Budinger

Research output: Contribution to journalArticle

138 Citations (Scopus)

Abstract

Summary: Dynamic positron emission tomography with [18F)fluorodeoxyglucose was used in six patients with Alzheimer's disease (AD) and seven healthy age-matched control subjects to estimate the kinetic parameters K1*, k2*, and k3* that describe glucose transport and phosphorylation. A high-resolution tomograph was used to acquire brain uptake data in one tomographic plane, and a radial artery catheter connected to a plastic scintillator was used to acquire arterial input data. A nonlinear iterative least-squares fitting procedure that included terms for the vascular fraction and time delay to the peripheral sampling site was used to fit a three-compartment model to the brain data. Regions studied included frontal, temporal, occipital, and the entire cortex and subcortical white matter. The values obtained for the individual rate constants and regional CMRglc (rCMRglc; calculated using regional values of the rate constants) were higher than those reported previously. A significant (p < 0.05) decrease was found in K1* in frontal and temporal cortex in the AD patients compared with the controls, with values of 0.157 and 0.161 ml/g/min in frontal and temporal cortex, respectively, of controls and 0.127 and 0.126 ml/g/min in frontal and temporal cortex of the AD patients. rCMRglc was also significantly (p < 0.02) lower in the AD patients than controls in all cortical brain regions. Lower values of k3* were found in all brain regions in the AD patients, although these were not statistically significant. These findings provide evidence of an in vivo abnormality of forward glucose transport in AD. This transport defect, however, is probably not the cause of the diminution in glucose metabolism that has been widely found in AD patients, since a diminution of this magnitude should not lower intracerebral glucose content enough to alter rCM-Rglc.

Original languageEnglish (US)
Pages (from-to)323-330
Number of pages8
JournalJournal of Cerebral Blood Flow and Metabolism
Volume11
Issue number2
StatePublished - 1991

Fingerprint

Alzheimer Disease
Glucose
Frontal Lobe
Temporal Lobe
Brain
Occipital Lobe
Radial Artery
Fluorodeoxyglucose F18
Least-Squares Analysis
Positron-Emission Tomography
Plastics
Blood Vessels
Catheters
Phosphorylation

Keywords

  • Alzheimer's disease
  • Glucose metabolism
  • Glucose transport
  • Positron emission tomography

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Neuroscience(all)

Cite this

Jagust, W. J., Seab, J. P., Huesman, R. H., Valk, P. E., Mathis, C. A., Reed, B. R., ... Budinger, T. F. (1991). Diminished glucose transport in alzheimer's disease: Dynamic PET studies. Journal of Cerebral Blood Flow and Metabolism, 11(2), 323-330.

Diminished glucose transport in alzheimer's disease : Dynamic PET studies. / Jagust, William J.; Seab, J. Philip; Huesman, Ronald H.; Valk, Peter E.; Mathis, Chester A.; Reed, Bruce R; Coxson, Pamela G.; Budinger, Thomas F.

In: Journal of Cerebral Blood Flow and Metabolism, Vol. 11, No. 2, 1991, p. 323-330.

Research output: Contribution to journalArticle

Jagust, WJ, Seab, JP, Huesman, RH, Valk, PE, Mathis, CA, Reed, BR, Coxson, PG & Budinger, TF 1991, 'Diminished glucose transport in alzheimer's disease: Dynamic PET studies', Journal of Cerebral Blood Flow and Metabolism, vol. 11, no. 2, pp. 323-330.
Jagust, William J. ; Seab, J. Philip ; Huesman, Ronald H. ; Valk, Peter E. ; Mathis, Chester A. ; Reed, Bruce R ; Coxson, Pamela G. ; Budinger, Thomas F. / Diminished glucose transport in alzheimer's disease : Dynamic PET studies. In: Journal of Cerebral Blood Flow and Metabolism. 1991 ; Vol. 11, No. 2. pp. 323-330.
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