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Cited by 140Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

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Aging-related down-regulation of neprilysin, a putative β-amyloid-degrading enzyme, in transgenic Tg2576 Alzheimer-like mouse brain is accompanied by an astroglial upregulation in the vicinity of β-amyloid plaques

Apelt, Jenny, Ach, Katrin, Schliebs, Reinhard·2003·Neuroscience Letters
DOI 10.1016/s0304-3940(03)00030-2
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Abstract

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-amyloid 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.

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  • Apoe-deficient astrocytes upregulate genes associated with inhibition of Aβ fibrillization (Ptgds and Cst3) and regulation of protein degradation (Ubb, Ubc and Ctsl).

    “Interestingly, Apoe-deficient astrocytes upregulate genes associated with inhibition of Aβ fibrillization (Ptgds and Cst3) and regulation of protein degradation (Ubb, Ubc and Ctsl) (Apelt et al, 2003; Davis et al, 2021; Liu et al, 2017a; Wegiel et al, 2000).”

    From APOE from astrocytes restores Alzheimer’s Aβ-pathology and DAM-like responses in APOE deficient microglia (2024) · cites this paper as Apelt et al, 2003

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Research works printed but not linked: 16

  1. Akiyama, 2001, Immunohistochemical localization of neprilysin in the human cerebral cortex: inverse association with vulnerability to amyloid β-protein (Aβ) deposition, Brain Res., 902, 277, 10.1016/S0006-8993(01)02390-3 · DOI
  2. Apelt, 2001, β-amyloid-induced glial expression of both pro- and anti-inflammatory cytokines in cerebral cortex of aged transgenic Tg2576 mice with Alzheimer plaque pathology, Brain Res., 894, 21, 10.1016/S0006-8993(00)03176-0 · DOI · Paper page
  3. Apelt, 2002, Impairment of cholinergic neurotransmission in adult and aged transgenic Tg2576 mouse brain expressing the Swedish mutation of human β-amyloid precursor protein, Brain Res., 953, 17, 10.1016/S0006-8993(02)03262-6 · DOI
  4. Carson, 2002, Beta-amyloid catabolism: roles for neprilysin (NEP) and other metallopeptidases?, J. Neurochem., 81, 1, 10.1046/j.1471-4159.2002.00855.x · DOI
  5. Fukami, 2002, Aβ-degrading endopeptidase, neprilysin, in mouse brain: synaptic and axonal localization inversely correlating with Abeta pathology, Neurosci. Res., 43, 39, 10.1016/S0168-0102(02)00015-9 · DOI · Paper page
  6. Hsiao, 1996, Correlative memory deficits, Aβ elevation, and amyloid plaques in transgenic mice, Science, 274, 99, 10.1126/science.274.5284.99 · DOI · Paper page
  7. Iwata, N., Takaki, Y., Fukami, S., Tsubuki, S., Sekiguchi, M., Watanabe, K, Hosokoi, E. and Saido, T.C., Region-specific reduction of Aβ-degrading endopetidase, neprilysin, in mouse hippocampus upon aging, Program No. 688.15. 2002, Abstract Viewer/Itinerary Planner, Society for Neuroscience, Washington, DC (2002) Online. · DOI
  8. Iwata, 2001, Metabolic regulation of brain Aβ by neprilysin, Science, 292, 1550, 10.1126/science.1059946 · DOI
  9. Iwata, 2000, Identification of the major Aβ1-42-degrading catabolic pathway in brain parenchyma: suppression leads to biochemical and pathological deposition, Nat. Med., 6, 143, 10.1038/77399 · DOI
  10. Li, 1995, Tissue-specific expression of rat neutral endopeptidase (neprilysin) mRNAs, J. Biol. Chem., 270, 5723, 10.1074/jbc.270.11.5723 · DOI
  11. Li, 1998, Characterization of the promoter region of the rat neprilysin gene, Arch. Biochem. Biophys., 358, 189, 10.1006/abbi.1998.0855 · DOI
  12. Mohajeri, 2002, Aβ42-induced increase in neprilysin is associated with prevention of amyloid plaque formation in vivo, J. Biol. Chem., 277, 35460, 10.1074/jbc.M202899200 · DOI
  13. Selkoe, 2001, Clearing the brains amyloid cobwebs, Neuron, 32, 177, 10.1016/S0896-6273(01)00475-5 · DOI · Paper page
  14. Turner, 2001, The neprilysin (NEP) family of zinc metalloendopeptidases: genomics and function, BioEssays, 23, 261, 10.1002/1521-1878(200103)23:3<261::AID-BIES1036>3.0.CO;2-K · DOI
  15. Yasojima, 2001, Relationship between β-amyloid peptide generating molecules and neprilysin in Alzheimer disease and normal brain, Brain Res., 919, 115, 10.1016/S0006-8993(01)03008-6 · DOI
  16. Yasojima, 2001, Reduced neprilysin in high plaque areas of Alzheimer brain: a possible relationship to deficient degradation of β-amyloid peptide, Neurosci. Lett., 297, 97, 10.1016/S0304-3940(00)01675-X · DOI

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Metadata

Authors
Apelt, J., Ach, K., & Schliebs, R.
Affiliations
Leipzig University (DE)
Corresponding author
Schliebs, Reinhard
Venue
Neuroscience Letters
Publisher
Elsevier BV
Published
2003-03
Volume
339
Issue
3
Pages
183-186
ISSN
0304-3940 (ISSN-L)
DOI
10.1016/s0304-3940(03)00030-2
OpenAlex
W1967794260
Cited by
140
References
0
Citations by year
2026: 3 · 2025: 4 · 2024: 4 · 2023: 8 · 2022: 6 · 2021: 4 · 2020: 5 · 2019: 5 · 2018: 3 · 2017: 6 · 2016: 4 · 2015: 7 · 2014: 11 · 2013: 7 · 2012: 7
FWCI
5.74
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Neuroscience Letters (publishedVersion)
  • PubMed (publishedVersion)
Funders
Bundesministerium für Bildung und Forschung
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
neprilysin, amyloid-beta, Alzheimer's disease, Tg2576 mice, amyloid plaques, astrocyte activation, reactive astrocytes, aging, zinc metalloprotease, cerebral cortex, dystrophic neurites, postnatal maturation
MeSH terms
Aging, Alzheimer Disease, Animals, Astrocytes, Brain, Humans, Mice, Inbred C57BL, Mice, Transgenic, Neprilysin, Down-Regulation, Up-Regulation, Amyloid beta-Peptides, Mice, Plaque, Amyloid

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