Premium
P3‐232: The role of c‐Abl in the synaptotoxicity caused by Aβ oligomers: Involvement of the ephrine receptor
Author(s) -
Alvarez Alejandra
Publication year - 2011
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2011.05.1674
Subject(s) - dendritic spine , abl , microbiology and biotechnology , synaptic plasticity , tyrosine kinase , receptor tyrosine kinase , chemistry , tyrosine , phosphorylation , hippocampal formation , tyrosine phosphorylation , postsynaptic potential , long term potentiation , biology , neuroscience , signal transduction , receptor , biochemistry
Alterations in synaptic function and structure are one of the early events in Alzheimer disease. Specifically, it has been showed that Aβ oligomers induced a decreased in dendritic spines, synaptic loss, plasticity alterations and cognitive damage. However, the molecular mechanisms activated by Aβ oligomers leading to synaptic dysfunction and loss have not been completely explained. In our laboratory we described that Aβ fibers induce c-Abl activation and this kinase is present in both pre and post synaptic structures. Has been described that the tyrosine kinase receptor ephrine A4 (EphA4) is able to interact with c-Abl and this interaction allows the reciprocal tyrosine phosphorylation.