Journal
NEUROSCIENCE LETTERS
Volume 339, Issue 3, Pages 183-186Publisher
ELSEVIER SCI IRELAND LTD
DOI: 10.1016/S0304-3940(03)00030-2
Keywords
neprilysin; beta-amyloid catabolism; Alzheimer's disease; immunocytochemistry; transgenic amyloid precursor protein(sw) mouse brain
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Pathological accumulation of cortical beta-amyloid is an early and consistent feature of Alzheimer's disease. Brain level of beta-amyloid is determined both by its production and by its catabolism. Neprilysin, a zinc metalloproteinase has been suggested as potential candidate of beta-amyloid-degrading enzyme in vivo. To address the question whether pathological accumulation of beta-arnyloid peptides in transgenic Tg2576 mice with Alzheimer-like pathology may affect beta-amyloid catabolism, the expression of neprilysin was studied during postnatal maturation and aging. Neprilysin protein but mRNA levels decreased in mouse cerebral cortex with age (2-22 months), independently of transgene status. Immunocytochemistry revealed few neprilysin-positive dystrophic neurites around beta-amyloid plaques and an upregulation of neprilysin in plaque-surrounding reactive astrocytes which may suggest a role of plaque-mediated astrogliosis in beta-amyloid degradation. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved.
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