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The nuclear cofactor receptor interacting protein-140 (RIP140) regulates the expression of genes involved in Aβ

Katrin Blondrath1, Jennifer H Steel2, Loukia Katsouri1

  • 1Division of Brain Sciences, Department of Medicine, Imperial College London, London, UK.

Neurobiology of Aging
|September 11, 2016
PubMed

Insights

Receptor interacting protein-140 (RIP140) levels are reduced in Alzheimer's disease (AD) brains. RIP140 may protect against AD by reducing amyloid-beta (Aβ) generation through a PPARγ-dependent mechanism.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Receptor interacting protein-140 (RIP140) is a cofactor regulating metabolic and inflammatory genes.
  • RIP140's role in Alzheimer's disease (AD) pathogenesis is unknown, but it modulates transcription factors like PPARγ involved in amyloid precursor protein (APP) processing.

Purpose of the Study:

  • To investigate the role of RIP140 in Alzheimer's disease (AD) and its potential impact on amyloid-beta (Aβ) generation.

Main Methods:

  • Examined RIP140 levels in postmortem AD brains versus controls.
  • Used in situ hybridization to determine RIP140 expression patterns in AD-affected brain regions.
  • Employed cell lines and genetically modified mice to study RIP140's effect on AD-related gene transcription (BACE1, GSK3).

Main Results:

  • RIP140 levels were decreased in AD brains.
  • RIP140 expression was enriched in the cortex and hippocampus, areas affected by AD pathology.
  • RIP140 modulated the transcription of BACE1 and GSK3.
  • RIP140 overexpression reduced Aβ generation in neuroblastoma cells by decreasing BACE1 transcription via a PPARγ-dependent pathway.

Conclusions:

  • RIP140 is implicated in Alzheimer's disease (AD) pathology.
  • RIP140 may serve a protective role in AD by inhibiting amyloid-beta (Aβ) production.
  • Findings suggest a link between metabolic signaling pathways and AD pathogenesis.
Keywords:
Alzheimer's diseaseAβBACE1GSK3PPARγRIP140

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