Cited by 40Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Transcriptional and post‐transcriptional regulation of β‐secretase

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Tamagno, Elena, Guglielmotto, M., Monteleone, D., Vercelli, A., Tabaton, M.·2012·IUBMB Life

Abstract

Alzheimer's disease (AD) is a devastating neurodegenerative disorder that results in loss of memory and cognitive function, eventually leading to dementia. A key neuropathological event in AD is the cerebral accumulation of senile plaques formed by aggregates of amyloid-β-peptides (Aβ). Aβ results from two sequential endoproteolytic cleavages operated on the amyloid-β precursor protein (AβPP), an integral membrane protein with a single-membrane spanning domain, a large extracellular N-terminus and a shorter, cytoplasmic C-terminus. First, β-secretase (BACE1) cleaves AβPP at the N-terminal end of the Aβ sequence to produce a secreted form of AβPP, named sAβPP, and a C-terminal membrane-bound 99-aminoacid fragment (C99). Then, γ-secretase cleaves C99 within the transmembrane domain to release the Aβ peptides of different lengths, predominantly Aβ1-40 and Aβ1-42.

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Crossref · 10.1002/iub.1099

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  • Both oxidative stress and inflammation increase BACE1 expression.

    “Interestingly, several studies have suggested that both oxidative stress and inflammation increase BACE1 expression (Chami & Checler 2012, Rossner et al. 2006, Tamagno et al. 2012).”

    From miR‐186 is decreased in aged brain and suppresses <scp>BACE</scp>1 expression (2016) · cites this paper as Tamagno et al. 2012

  • BACE1 expression is up-regulated by oxidative stress and inflammation.

    “Although BACE1 expression has been known to be up-regulated by oxidative stress and inflammation (Chami & Checler 2012, Rossner et al. 2006, Tamagno et al. 2012), our data suggest that miR-186 does not mediate the BACE1 induction by those aging-associated stresses.”

    From miR‐186 is decreased in aged brain and suppresses <scp>BACE</scp>1 expression (2016) · cites this paper as Tamagno et al. 2012

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Authors
Tamagno, E., Guglielmotto, M., Monteleone, D., Vercelli, A., & Tabaton, M.
Affiliations
  • Neuroscience Institute Cavalieri Ottolenghi (IT)
  • University of Genoa (IT)
Corresponding author
Tamagno, Elena
Venue
IUBMB Life
Publisher
Wiley
Published
2012-11-26
Volume
64
Issue
12
Pages
943-950
ISSN
  • 1521-6543 (ISSN-L)
  • 1521-6551
OpenAlex
W2011885084
Cited by
40
References
114
Citations by year
2025: 4 · 2024: 1 · 2023: 4 · 2022: 2 · 2021: 3 · 2020: 4 · 2019: 3 · 2018: 2 · 2017: 3 · 2016: 7 · 2015: 4 · 2014: 1 · 2013: 1
FWCI
0.21
Type
journal article
Language
en
Open access
Locations
  • IUBMB Life (publishedVersion)
  • PubMed (publishedVersion)
  • Institutional Research Information System University of Turin (University of Turin) (submittedVersion, other-oa)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
beta-secretase, BACE1, Alzheimer's disease, amyloid precursor protein, amyloid-beta, transcriptional regulation, post-transcriptional regulation, amyloid plaques, gamma-secretase, C99
MeSH terms
Alzheimer Disease, Brain, Humans, Peptide Fragments, RNA Processing, Post-Transcriptional, RNA, Messenger, Transcription, Genetic, Signal Transduction, Aspartic Acid Endopeptidases, Amyloid beta-Protein Precursor, Protein Structure, Tertiary, Amyloid Precursor Protein Secretases, Plaque, Amyloid, Proteolysis

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