Biochemical measurements in Alzheimer's disease reveal a necessity for improved neuroimaging techniques to study metabolism.
A series of Alzheimer's disease and control brains were dissected to determine the extent of atrophy (based on total protein content) and loss of choline acetyltransferase activity in the cerebral cortex from the entire surface of the diseased brains. The distribution of intensity of pathology so determined is strikingly similar to the degree of hypometabolism as shown by positron emission tomography. It is argued that the hypometabolism can be explained (at least in part) by focal areas of atrophy.
Najlerahim
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Miriam Marks Department of Neurochemistry, University of London, U.K.
Bowen
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D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology; D001284:Atrophy / Q000378:metabolism; D002540:Cerebral Cortex / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D005260:Female; D006801:Humans; D008875:Middle Aged; D009419:Nerve Tissue Proteins / Q000378:metabolism; D014018:Tissue Distribution
D009419:Nerve Tissue Proteins; D002795:Choline O-Acetyltransferase