Abnormalities of the glucose transporter at the blood-brain barrier and in brain in Alzheimer's disease.
We have previously demonstrated the glucose transporter (GT) by [3H]cytochalasin B binding and immunocytochemistry in brain and in cerebral microvessels which form the blood-brain barrier. In this study, we assessed the GT protein in the frontal cortex, hippocampus, cerebellum, and cerebral microvessels in subjects with Alzheimer's disease (AD) and controls. In AD, we found a marked decrease in the GT in brain microvessels and in the frontal cortex and hippocampus, regions that are classically affected in AD, but there were no significant changes in the cerebellum. The binding of [3H]cytochalasin B to frontal cortex was not correlated with age or with the interval between death and autopsy. The impairment of GT in cerebral microvessels and cortex in AD subjects is relatively specific and appears to be disease-related. Our findings may be associated with the decreased in vivo measurements of cerebral oxidative metabolism in AD.
Kalaria
R N
RN
Department of Neurology, University Hospitals of Cleveland, Ohio.
Harik
S I
SI
D000368:Aged; D000544:Alzheimer Disease / Q000378:metabolism* / Q000503:physiopathology; D001812:Blood-Brain Barrier; D001921:Brain / Q000098:blood supply / Q000378:metabolism*; D006801:Humans; D008833:Microcirculation; D009004:Monosaccharide Transport Proteins / Q000378:metabolism*
D009004:Monosaccharide Transport Proteins