Reduced glucose transporter at the blood-brain barrier and in cerebral cortex in Alzheimer disease.
We studied the hexose transporter protein of the frontal and temporal neocortex, hippocampus, putamen, cerebellum, and cerebral microvessels (which constitute the blood-brain barrier) in Alzheimer disease and control subjects by reversible and covalent binding with [3H]cytochalasin B and by immunological reactivity. In Alzheimer disease subjects, we found a marked decrease in the hexose transporter in brain microvessels and in the cerebral neocortex and hippocampus, regions that are most affected in Alzheimer disease, but there were no abnormalities in the putamen or cerebellum. Hexose transporter reduction in cerebral microvessels of Alzheimer subjects is relatively specific because other enzyme markers of brain endothelium were not significantly altered. The low density of the hexose transporter at the blood-brain barrier and in the cerebral cortex in Alzheimer disease may be related to decreased in vivo measurements of cerebral oxidative metabolism.
Kalaria
R N
RN
Department of Neurology, University Hospitals of Cleveland, Ohio 44106.
Harik
S I
SI
D000328:Adult; D000368:Aged; D000375:Aging; D000544:Alzheimer Disease / Q000378:metabolism*; D001812:Blood-Brain Barrier; D002540:Cerebral Cortex / Q000254:growth & development / Q000378:metabolism*; D002560:Cerebrovascular Circulation; D003571:Cytochalasin B / Q000378:metabolism; D005260:Female; D006801:Humans; D007700:Kinetics; D008297:Male; D008833:Microcirculation / Q000378:metabolism; D009004:Monosaccharide Transport Proteins / Q000378:metabolism*; D012016:Reference Values
D009004:Monosaccharide Transport Proteins; D003571:Cytochalasin B