Glutamine synthetase (GS) expression is reduced in senile dementia of the Alzheimer type.
Glutamine synthetase (GS), a metabolic marker of the mature astrocyte, was investigated in the temporal neocortex of postmortem brain samples of 8 cases, either not demented or affected by senile dementia of the Alzheimer type. A negative correlation between the GS protein level and the density of both classical beta A4 deposits and senile plaques was evidenced. Such a correlation for GS underlies a dysfunction of the astroglial metabolism and particularly of the glutamate and ammonia neutralization. Since GS is sensitive to oxidative lesioning, the changes in GS level that were observed, occurring at the posttranslational stage, might reflect oxidative damage and have severe consequences on the pathological cascade of events.
D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000201:enzymology* / Q000378:metabolism / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000032:analysis / Q000378:metabolism; D001253:Astrocytes / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D001483:Base Sequence; D017931:DNA Primers; D005260:Female; D015870:Gene Expression; D005904:Glial Fibrillary Acidic Protein / Q000096:biosynthesis; D005974:Glutamate-Ammonia Ligase / Q000096:biosynthesis*; D006801:Humans; D008969:Molecular Sequence Data; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis*; D013702:Temporal Lobe / Q000201:enzymology* / Q000378:metabolism / Q000473:pathology
D016229:Amyloid beta-Peptides; D017931:DNA Primers; D005904:Glial Fibrillary Acidic Protein; D012333:RNA, Messenger; D005974:Glutamate-Ammonia Ligase