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To further assess the nature of the abnormality of KGDHC in AD, KGDHC activities and immunoreactivities were analyzed in brains from AD patients bearing the Swedish APP670\/671 mutation. This gene defect causes overproduction of the amyloid \u03b2 peptide. KGDHC activities were reduced by 55 to 57% compared with control values in the mutation\u2010bearing AD cases in the medial temporal and superior frontal cortices. The immunochemical levels of KGDHC subunits E1k (\u221251%) and E2k (\u221276%) declined, whereas E3 concentrations were unchanged. 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