Docosahexaenoic acid prevents neuronal apoptosis induced by soluble amyloid-β oligomers
Version of Record online: 21 NOV 2005
Journal of Neurochemistry
Volume 96, Issue 2, pages 385–395, January 2006
How to Cite
Florent, S., Malaplate-Armand, C., Youssef, I., Kriem, B., Koziel, V., Escanyé, M.-C., Fifre, A., Sponne, I., Leininger-Muller, B., Olivier, J.-L., Pillot, T. and Oster, T. (2006), Docosahexaenoic acid prevents neuronal apoptosis induced by soluble amyloid-β oligomers. Journal of Neurochemistry, 96: 385–395. doi: 10.1111/j.1471-4159.2005.03541.x
- Issue online: 21 NOV 2005
- Version of Record online: 21 NOV 2005
- Received June 13, 2005; accepted September 16, 2005.
- Alzheimer's disease;
- docosahexaenoic acid;
- neuronal apoptosis;
- soluble amyloid-β peptide
A growing body of evidence supports the notion that soluble oligomers of amyloid-β (Aβ) peptide interact with the neuronal plasma membrane, leading to cell injury and inducing death-signalling pathways that could account for the increased neurodegeneration occurring in Alzheimer's disease (AD). Docosahexaenoic acid (DHA, C22:6, n-3) is an essential polyunsaturated fatty acid in the CNS and has been shown in several epidemiological and in vivo studies to have protective effects against AD and cognitive alterations. However, the molecular mechanisms involved remain unknown. We hypothesized that DHA enrichment of plasma membranes could protect neurones from apoptosis induced by soluble Aβ oligomers. DHA pre-treatment was observed to significantly increase neuronal survival upon Aβ treatment by preventing cytoskeleton perturbations, caspase activation and apoptosis, as well as by promoting extracellular signal-related kinase (ERK)-related survival pathways. These data suggest that DHA enrichment probably induces changes in neuronal membrane properties with functional outcomes, thereby increasing protection from soluble Aβ oligomers. Such neuroprotective effects could be of major interest in the prevention of AD and other neurodegenerative diseases.