MicroRNA networks surrounding APP and amyloid-β metabolism

implications for Alzheimer's disease

Nicole Schonrock*, Miriam Matamales, Lars M. Ittner, Jürgen Götz

*Corresponding author for this work

Research output: Contribution to journalReview article

83 Citations (Scopus)

Abstract

MicroRNAs (miRNAs) are small non-coding RNA regulators of protein synthesis that function as "fine-tuning" tools of gene expression in development and tissue homeostasis. Their profiles are significantly altered in neurodegenerative diseases such as Alzheimer's disease (AD) that is characterized by both amyloid-β (Aβ) and tau deposition in brain. A key challenge remains in determining how changes in miRNA profiles translate into biological function in a physiological and pathological context. The key lies in identifying specific target genes for deregulated miRNAs and understanding which pathogenic factors trigger their deregulation. Here we review the literature about the intricate network of miRNAs surrounding the regulation of the amyloid precursor protein (APP) from which Aβ is derived by proteolytic cleavage. Normal brain function is highly sensitive to any changes in APP metabolism and miRNAs function at several steps to ensure that the correct APP end product is produced and in the right form and abundance. Disruptions in this miRNA regulatory network may therefore alter Aβ production, which in turn can affect miRNA expression.

Original languageEnglish
Pages (from-to)447-454
Number of pages8
JournalExperimental Neurology
Volume235
Issue number2
DOIs
Publication statusPublished - 1 Jun 2012
Externally publishedYes

Keywords

  • β-secretase
  • Aβ (amyloid-β)
  • Alzheimer
  • Animal model
  • APP (amyloid precursor protein)
  • BACE1
  • MicroRNA
  • Neurodegeneration
  • Splicing
  • Tau

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