Lack of evidence of the interaction of the Aß peptide with the Wnt signaling cascade in Drosophila models of Alzheimer's disease.

Détails

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Etat: Public
Version: de l'auteur
ID Serval
serval:BIB_0947EC3A5BCD
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Lack of evidence of the interaction of the Aß peptide with the Wnt signaling cascade in Drosophila models of Alzheimer's disease.
Périodique
Molecular Brain
Auteur(s)
Lüchtenborg A.M., Katanaev V.L.
ISSN
1756-6606 (Electronic)
ISSN-L
1756-6606
Statut éditorial
Publié
Date de publication
2014
Peer-reviewed
Oui
Volume
7
Numéro
1
Pages
81
Langue
anglais
Notes
Publication types: ARTICLE
Résumé
Background Alzheimer's disease (AD) is the leading form of dementia worldwide. The Aß-peptide is believed to be the major pathogenic compound of the disease. Since several years it is hypothesized that Aß impacts the Wnt signaling cascade and therefore activation of this signaling pathway is proposed to rescue the neurotoxic effect of Aß.
Findings Expression of the human Aß42 in the Drosophila nervous system leads to a drastically shortened life span. We found that the action of Aß42 specifically in the glutamatergic motoneurons is responsible for the reduced survival. However, we find that the morphology of the glutamatergic larval neuromuscular junctions, which are widely used as the model for mammalian central nervous system synapses, is not affected by Aß42 expression. We furthermore demonstrate that genetic activation of the Wnt signal transduction pathway in the nervous system is not able to rescue the shortened life span or a rough eye phenotype in Drosophila.
Conclusions Our data confirm that the life span is a useful readout of Aß42 induced neurotoxicity in Drosophila; the neuromuscular junction seems however not to be an appropriate model to study AD in flies. Additionally, our results challenge the hypothesis that Wnt signaling might be implicated in Aß42 toxicity and might serve as a drug target against AD.
Pubmed
Web of science
Open Access
Oui
Création de la notice
11/12/2014 18:05
Dernière modification de la notice
20/08/2019 12:31
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