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Apolipoprotein E-mimetics inhibit neurodegeneration and restore cognitive functions in a transgenic Drosophila model of Alzheimer's disease.

Publication ,  Journal Article
Sarantseva, S; Timoshenko, S; Bolshakova, O; Karaseva, E; Rodin, D; Schwarzman, AL; Vitek, MP
Published in: PLoS One
December 7, 2009

BACKGROUND: Mutations of the amyloid precursor protein gene (APP) are found in familial forms of Alzheimer's disease (AD) and some lead to the elevated production of amyloid-beta-protein (Abeta). While Abeta has been implicated in the causation of AD, the exact role played by Abeta and its APP precursor are still unclear. PRINCIPAL FINDINGS: In our study, Drosophila melanogaster transgenics were established as a model to analyze AD-like pathology caused by APP overexpression. We demonstrated that age related changes in the levels and pattern of synaptic proteins accompanied progressive neurodegeneration and impairment of cognitive functions in APP transgenic flies, but that these changes may be independent from the generation of Abeta. Using novel peptide mimetics of Apolipoprotein-E, COG112 or COG133 proved to be neuroprotective and significantly improved the learning and memory of APP transgenic flies. CONCLUSIONS: The development of neurodegeneration and cognitive deficits was corrected by injections of COG112 or COG133, novel mimetics of apolipoprotein-E (apoE) with neuroprotective activities.

Duke Scholars

Published In

PLoS One

DOI

EISSN

1932-6203

Publication Date

December 7, 2009

Volume

4

Issue

12

Start / End Page

e8191

Location

United States

Related Subject Headings

  • R-SNARE Proteins
  • Peptides
  • Nerve Degeneration
  • Memory
  • Humans
  • Green Fluorescent Proteins
  • General Science & Technology
  • Drosophila melanogaster
  • Disease Models, Animal
  • Cognition
 

Citation

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Sarantseva, S., Timoshenko, S., Bolshakova, O., Karaseva, E., Rodin, D., Schwarzman, A. L., & Vitek, M. P. (2009). Apolipoprotein E-mimetics inhibit neurodegeneration and restore cognitive functions in a transgenic Drosophila model of Alzheimer's disease. PLoS One, 4(12), e8191. https://doi.org/10.1371/journal.pone.0008191
Sarantseva, Svetlana, Svetlana Timoshenko, Olga Bolshakova, Eugenia Karaseva, Dmitry Rodin, Alexander L. Schwarzman, and Michael P. Vitek. “Apolipoprotein E-mimetics inhibit neurodegeneration and restore cognitive functions in a transgenic Drosophila model of Alzheimer's disease.PLoS One 4, no. 12 (December 7, 2009): e8191. https://doi.org/10.1371/journal.pone.0008191.
Sarantseva S, Timoshenko S, Bolshakova O, Karaseva E, Rodin D, Schwarzman AL, et al. Apolipoprotein E-mimetics inhibit neurodegeneration and restore cognitive functions in a transgenic Drosophila model of Alzheimer's disease. PLoS One. 2009 Dec 7;4(12):e8191.
Sarantseva, Svetlana, et al. “Apolipoprotein E-mimetics inhibit neurodegeneration and restore cognitive functions in a transgenic Drosophila model of Alzheimer's disease.PLoS One, vol. 4, no. 12, Dec. 2009, p. e8191. Pubmed, doi:10.1371/journal.pone.0008191.
Sarantseva S, Timoshenko S, Bolshakova O, Karaseva E, Rodin D, Schwarzman AL, Vitek MP. Apolipoprotein E-mimetics inhibit neurodegeneration and restore cognitive functions in a transgenic Drosophila model of Alzheimer's disease. PLoS One. 2009 Dec 7;4(12):e8191.

Published In

PLoS One

DOI

EISSN

1932-6203

Publication Date

December 7, 2009

Volume

4

Issue

12

Start / End Page

e8191

Location

United States

Related Subject Headings

  • R-SNARE Proteins
  • Peptides
  • Nerve Degeneration
  • Memory
  • Humans
  • Green Fluorescent Proteins
  • General Science & Technology
  • Drosophila melanogaster
  • Disease Models, Animal
  • Cognition