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Updated: Jul 27, 2026

Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain
10:08

Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain

Published on: August 28, 2012

MT5-MMP, just a new APP processing proteinase in Alzheimer's disease?

Kévin Baranger1, Michel Khrestchatisky1, Santiago Rivera2

  • 1Aix Marseille Univ, CNRS, NICN, Marseille, France.

Journal of Neuroinflammation
|June 29, 2016
PubMed

Insights

We identified membrane-type 5-MMP (MT5-MMP) in Alzheimer's disease (AD) models. This enzyme processes amyloid precursor protein (APP) and may worsen AD through inflammation and altered APP transport.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Molecular Biology

Background:

  • Alzheimer's disease (AD) pathogenesis involves amyloid precursor protein (APP) processing.
  • The role of specific proteases in AD is an area of active research.

Purpose of the Study:

  • To investigate the role of membrane-type 5-MMP (MT5-MMP) in Alzheimer's disease (AD).
  • To explore potential mechanisms by which MT5-MMP contributes to AD pathogenesis beyond APP processing.

Main Methods:

  • Utilized a transgenic mouse model of Alzheimer's disease (AD).
  • Investigated the enzymatic activity of MT5-MMP on amyloid precursor protein (APP).
  • Examined the potential involvement of inflammatory pathways and APP trafficking.

Main Results:

  • MT5-MMP was identified as a new factor in AD pathogenesis.
  • MT5-MMP exhibits pro-amyloidogenic properties and processes APP.
  • APP processing by MT5-MMP may release a neurotoxic fragment.
  • Hypothesized complementary roles for MT5-MMP in activating inflammation and altering APP trafficking.

Conclusions:

  • MT5-MMP is implicated in Alzheimer's disease (AD) pathogenesis.
  • MT5-MMP's role extends beyond direct APP processing, potentially involving inflammatory responses and APP transport.
  • Further research is warranted to elucidate the full impact of MT5-MMP in AD.
Keywords:
Amyloid precursor proteinAmyloidogenesisIL-1βMatrix metalloproteinasesNeurodegenerative diseaseNeuroinflammationTrafficking

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