|Citation||Finelli, A., Kelkar, A., Song, H.J., Yang, H., Konsolaki, M. (2004). A model for studying Alzheimer's Abeta42-induced toxicity in Drosophila melanogaster. Mol. Cell. Neurosci. 26(3): 365--375. (Export to RIS)|
|Publication Type||Research paper|
|PubMed Abstract||Alzheimer's disease is a neurological disorder resulting in the degeneration and death of brain neurons controlling memory, cognition and behavior. Although overproduction of Abeta peptides is widely considered a causative event in the disease, the mechanisms by which Abeta peptides cause neurodegeneration and the processes of Abeta clearance and degradation remain unclear. To address these issues, we have expressed the Abeta peptides in Drosophila melanogaster. We show that overexpression of Abeta42 peptides in the nervous system results in phenotypes associated with neuronal degeneration in a dose- and age-dependent manner. We further show that a mutation in a Drosophila neprilysin gene suppresses the Abeta42 phenotypes by lowering the levels of the Abeta42 peptide, supporting the role of neprilysin in the catabolism of Abeta peptides in vivo. We propose that our Drosophila model is suitable for the study and elucidation of Abeta metabolism and toxicity at the genetic level.|
What does this section display?
This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms).
What does this section not display?
This section does not currently display links that were removed or gene model changes.
Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
|All updates||Click here to see a list of all updates to this record from FB2010_08 and on.|
|Language of Publication||English|
|Additional Languages of Abstract|
|Also Published As|
|Abbreviation||Mol. Cell. Neurosci.|
|Title||Molecular and Cellular Neurosciences|
|Data from Reference|
|Natural transposons (1)|