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Studying the pathogenesis of Alzheimer's disease in a Drosophila melanogaster model: Human APP overexpression in the brain of transgenic flies leads to deficit of the synaptic protein synaptotagmin

Publication ,  Journal Article
Sarantseva, SV; Bolshakova, OI; Timoshenko, SI; Rodin, DI; Vitek, M; Schwarzman, AL
Published in: Russian Journal of Genetics
January 1, 2009

Alzheimer's disease (AD) is a progressive neurodegenerative disease whose main pathomorphological sign is synapse degeneration in the cortex and hippocampus. Abnormal synaptogenesis precedes amyloidosis and neurodegeneration and correlates with memory impairment during the early clinical phase. Mutations in the amyloid precursor protein (APP) gene cause familial AD and enhance the secretion of amyloid-β protein (Aβ). However, it remains unclear in what way APP and Aβ- are involved in synaptic disorder in the absence of visible amyloid structures. In this study, the role of the human APP gene in synaptogenesis in transgenic lines of Drosophila melanogaster whose nerve cells express the human APP695 isoform, truncated APPs, and the presynaptic marker synaptotagmin containing the green fluorescent protein (GFP) sequence. The expression of APP and its truncated forms caused a decrease in the synaptotagmin content of antennal lobes (ALs) and mushroom bodies (MBs) of the D. melanogaster brain, as well as neurodegeneration that progressed with age. The results suggest that abnormal synaptogenesis and neurodegeneration occur in the Drosophila brain in the absence of β-. It is assumed that impaired cellular functions of APP and secretion of β- independently contribute to the pathogenesis of AD. © 2009 MAIK Nauka.

Duke Scholars

Published In

Russian Journal of Genetics

DOI

EISSN

1608-3369

ISSN

1022-7954

Publication Date

January 1, 2009

Volume

45

Issue

1

Start / End Page

105 / 112

Related Subject Headings

  • Genetics & Heredity
  • 3105 Genetics
  • 0604 Genetics
 

Citation

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ICMJE
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Sarantseva, S. V., Bolshakova, O. I., Timoshenko, S. I., Rodin, D. I., Vitek, M., & Schwarzman, A. L. (2009). Studying the pathogenesis of Alzheimer's disease in a Drosophila melanogaster model: Human APP overexpression in the brain of transgenic flies leads to deficit of the synaptic protein synaptotagmin. Russian Journal of Genetics, 45(1), 105–112. https://doi.org/10.1134/S1022795409010153
Sarantseva, S. V., O. I. Bolshakova, S. I. Timoshenko, D. I. Rodin, M. Vitek, and A. L. Schwarzman. “Studying the pathogenesis of Alzheimer's disease in a Drosophila melanogaster model: Human APP overexpression in the brain of transgenic flies leads to deficit of the synaptic protein synaptotagmin.” Russian Journal of Genetics 45, no. 1 (January 1, 2009): 105–12. https://doi.org/10.1134/S1022795409010153.
Sarantseva SV, Bolshakova OI, Timoshenko SI, Rodin DI, Vitek M, Schwarzman AL. Studying the pathogenesis of Alzheimer's disease in a Drosophila melanogaster model: Human APP overexpression in the brain of transgenic flies leads to deficit of the synaptic protein synaptotagmin. Russian Journal of Genetics. 2009 Jan 1;45(1):105–12.
Sarantseva, S. V., et al. “Studying the pathogenesis of Alzheimer's disease in a Drosophila melanogaster model: Human APP overexpression in the brain of transgenic flies leads to deficit of the synaptic protein synaptotagmin.” Russian Journal of Genetics, vol. 45, no. 1, Jan. 2009, pp. 105–12. Scopus, doi:10.1134/S1022795409010153.
Sarantseva SV, Bolshakova OI, Timoshenko SI, Rodin DI, Vitek M, Schwarzman AL. Studying the pathogenesis of Alzheimer's disease in a Drosophila melanogaster model: Human APP overexpression in the brain of transgenic flies leads to deficit of the synaptic protein synaptotagmin. Russian Journal of Genetics. 2009 Jan 1;45(1):105–112.
Journal cover image

Published In

Russian Journal of Genetics

DOI

EISSN

1608-3369

ISSN

1022-7954

Publication Date

January 1, 2009

Volume

45

Issue

1

Start / End Page

105 / 112

Related Subject Headings

  • Genetics & Heredity
  • 3105 Genetics
  • 0604 Genetics