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Alzheimer’s disease: how amyloid aggregates alter neuronal function - Cell Reports, May 2018

Tuesday 12 June 2018, by Marie-Noelle Gouineau

The accumulation of amyloid peptides in the form of plaques in the brain is one of the primary indicators of Alzheimer’s disease. While the harmful effects of amyloid peptide aggregates are well established, the mechanism through which they act on brain cells remains ill-defined. Researchers from CNRS and université de Bordeaux have just revealed that they alter the usual functioning of connections between neurons by interacting with a key enzyme of synaptic plasticity.
The results are published on June 12, 2018 in the journal Cell Reports.


Fig. Rat hippocampal neurons in primary culture, showing a fluorescent soluble protein (left) and trajectories corresponding to the movement of the glutamate receptors on its surface, measured by following individual molecules.

Contact: Daniel Choquet

- See the CNRS press release in English and in French

CaMKII metaplasticity drives Aβ oligomers-mediated synaptotoxicity.
P. Opazo, S. Viana da Silva, M.Carta, C. Breillat, S. J. Coultrap, D. Grillo-Bosch, M. Sainlos, F. Coussen, K. U. Bayer, C. Mulle, D. Choquet.
Cell Reports, June 12, 2018.

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