Article
Expression of A2V-mutated Aβ in Caenorhabditis elegans results in oligomer formation and toxicity.
Neurobiology of disease - 1 Feb 2014
Diomede Luisa, Di Fede Giuseppe, Romeo Margherita, Bagnati Renzo, Ghidoni Roberta, Fiordaliso Fabio, Salio Monica, Rossi Alessandro, Catania Marcella, Paterlini Anna, Benussi Luisa, Bastone Antonio, Stravalaci Matteo, Gobbi Marco, Tagliavini Fabrizio, Salmona Mario
Abstract excerpt
Although Alzheimer's disease (AD) is usually sporadic, in a small proportion of cases it is familial and can be linked to mutations in β-amyloid precursor protein (APP). Unlike the other genetic defects, the mutation [alanine-673→valine-673] (A673V) causes the disease only in the homozygous condition with enhanced amyloid β (Aβ) production and aggregation; heterozygous carriers remain unaffected. It is not clear...
Topics
- Amyloid beta-Peptides
- Animals
- Animals, Genetically Modified
- Caenorhabditis elegans
- Humans
- Locomotion
- Mutation
- Neurons
- Peptide Fragments