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RNA editing is a post-transcriptional modification where a precursor mRNA (pre-mRNA) nucleotide sequence is changed by base insertion, deletion, or modification. The extent of RNA editing varies from a few hundred bases, in mitochondrial DNA of trypanosomes, to a just single base, in nuclear genes of mammals. Even a single base change in the pre-mRNA can convert a codon for one amino acid into the codon for another amino acid or a stop codon. This type of re-coding can significantly affect the...

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Human apolipoprotein C-I expression in mice impairs learning and memory functions.

Karlygash Abildayeva1, Jimmy F P Berbée, Arjan Blokland

  • 1Department of Molecular Cell Biology and Department of Basic Neurosciences, European Graduate School of Neuroscience, Institute Brain and Behavior, University of Maastricht, Maastricht, The Netherlands.

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|December 28, 2007
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Summary

The H2 allele of APOC1 increases apolipoprotein C-I (apoC-I) expression, a risk factor for Alzheimer's disease (AD). Human apoC-I expression in mice impairs learning and memory, independent of apoE, suggesting a role in AD development.

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Area of Science:

  • Neuroscience
  • Genetics
  • Biochemistry

Background:

  • The APOC1 H2 allele increases apolipoprotein C-I (apoC-I) expression and is linked to Alzheimer's disease (AD).
  • ApoC-I protein is found in human brain astrocytes and endothelial cells, co-localizing with amyloid plaques in AD brains.

Purpose of the Study:

  • To investigate the role of apoC-I in Alzheimer's disease pathogenesis and cognitive function.
  • To determine if human apoC-I expression impairs cognitive functions in vivo.

Main Methods:

  • Examined apoC-I localization in human control and AD brains.
  • Performed in vitro experiments on amyloid-beta (Abeta) aggregation and neuronal death.
  • Utilized human APOC1 transgenic mice (hAPOC1(+/0)) to assess cognitive performance.

Main Results:

  • In vitro, apoC-I delayed Abeta aggregation but exacerbated soluble Abeta oligomer-induced neuronal death.
  • hAPOC1(+/0) mice showed impaired hippocampal-dependent learning and memory in object recognition and Morris water maze tasks.
  • No differences in endogenous apoE levels were observed between transgenic and wild-type mice.

Conclusions:

  • Human apoC-I expression impairs cognitive functions in mice independently of apoE.
  • ApoC-I may play a modulatory role in the development of Alzheimer's disease.