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March 1995

Positron Emission Tomography Measures of Benzodiazepine Binding in Alzheimer's Disease

Author Affiliations

From the Division of Nuclear Medicine, Department of Internal Medicine (Drs Meyer, Koeppe, Frey, and Kuhl), and the Department of Neurology (Drs Frey and Foster), The University of Michigan Medical Center, Ann Arbor.

Arch Neurol. 1995;52(3):314-317. doi:10.1001/archneur.1995.00540270110027

Objective:  To evaluate the integrity of neurons and neuropil in metabolically affected association cortices of patients with Alzheimer's disease by measuring central benzodiazepine binding sites with the use of positron emission tomography.

Design:  In patients with Alzheimer's disease, we determined the cerebral distribution of flumazenil tagged with carbon 11 ([11C]flumazenil), a ligand that binds to the gamma-aminobutyric acid A (GABAA) receptor complex, and the distribution of fludeoxyglucose tagged with fluorine 18 fludeoxyglucose F 18), a measure of local cerebral glucose metabolism. Tracer kinetic analysis was applied to quantify data in regions of interest. These data were compared with those of normal control subjects.

Subjects:  Patients with probable Alzheimer's disease ([11C]flumazenil, n=13; fludeoxyglucose F 18, n=11) and normal elderly control subjects ([11C]flumazenil, n=6; fludeoxyglucose F 18, n=10).

Results:  Significant decreases of the [11C]flumazenil transport rate were found in hypometabolic parietal and temporal association cortices, but [11C]flumazenil binding was not significantly decreased.

Conclusions:  When measured in living patients, association cortical benzodiazepine binding sites are relatively preserved, suggesting structurally intact cortical neuropil underlying the glucose hypometabolism identified in Alzheimer's disease.

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