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Identification and characterisation of the novel amyloid-beta peptide-induced protein p17

Saheen Nehar1, Manisha Mishra, Klaus Heese

  • 1Department of Molecular and Cell Biology, School of Biological Sciences, College of Science, Nanyang Technological University, 60 Nanyang Drive, Singapore 637551, Singapore.

FEBS Letters
|September 17, 2009
PubMed

Insights

Researchers identified a novel protein, p17, that is upregulated in Alzheimer's disease (AD). P17 inhibits crucial survival pathways and enhances amyloid precursor protein, suggesting its role in AD neurodegeneration.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Amyloid-beta peptide (Abeta) causes neurodegeneration via poorly understood mechanisms.
  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by Abeta accumulation.

Purpose of the Study:

  • To elucidate the mechanisms of Abeta-mediated neurotoxicity.
  • To characterize the novel gene p17 and its role in AD pathogenesis.

Main Methods:

  • cDNA subtraction analysis of Abeta-treated neuronal cells.
  • Characterization of p17 protein in cell lines (localization, function, expression).
  • Investigation of p17's interaction with protein kinase C and the TrkB-BDNF pathway.

Main Results:

  • A novel gene, p17, was found to be upregulated by Abeta and elevated in an AD mouse model.
  • P17 acts downstream of protein kinase C.
  • P17 inhibits the tyrosine receptor kinase B-brain-derived neurotrophic factor (TrkB-BDNF) pathway.
  • P17 impedes survival factors and enhances amyloid precursor protein (APP) expression.

Conclusions:

  • P17 is implicated in Abeta-mediated pro-apoptotic pathways in Alzheimer's disease.
  • P17 represents a potential therapeutic target for AD by modulating neurotoxic pathways.

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