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Sarantseva, S., Timoshenko, S., Bolshakova, O., Ka raseva, E., Rodin, D., Schwarzman, A.L. and Vitek, M.P. (2009) Apolipoprotein Emimetics inhibit neurodegen eration and restore cognitive functions in a transgenic Drosophila model of Alzheimer’s disease. PLOS One, 7, e8191. http://dx.doi.org/10.1371/journal.pone.0008191

has been cited by the following article:

• TITLE: Morphological abnormalities in Drosophila with overexpression of human APP gene

  AUTHORS: Dmitry Rodin, Olga Bolshakova, Galina Kislik, Svetlana Sarantseva

  KEYWORDS: Alzheimer’s Disease; Drosophila; Amyloid Precursor Protein; Morphological Abnormalities

  JOURNAL NAME: Open Journal of Animal Sciences, Vol.3 No.4B, November 18, 2013

  ABSTRACT: Alzheimer’s disease (AD) is the leading and one of the most severe forms of dementia. Molecular mechanisms underlying AD pathogenesis despite much work on this subject still remain unclear. Cleavage of amyloid precursor protein (APP) to amyloid beta peptide (A-beta) and following formation of amyloid plaques are the key events of Alzheimer’s pathology. Thus changes in APP expression and metabolism can lead to pathology development. Here we show that overexpression of human APP in Drosophila neural cells manifests in different morphological abnormalities of Drosophila imago that can be observed immediately after fly eclosion. This observation can help to further understand APP molecular functions and its participation in different molecular pathways.