Title |
Reduced sphingosine kinase-1 and enhanced sphingosine 1-phosphate lyase expression demonstrate deregulated sphingosine 1-phosphate signaling in Alzheimer’s disease
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Published in |
Acta Neuropathologica Communications, January 2014
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DOI | 10.1186/2051-5960-2-12 |
Pubmed ID | |
Authors |
Johnatan Ceccom, Najat Loukh, Valérie Lauwers-Cances, Christian Touriol, Yvan Nicaise, Catherine Gentil, Emmanuelle Uro-Coste, Stuart Pitson, Claude Alain Maurage, Charles Duyckaerts, Olivier Cuvillier, Marie-Bernadette Delisle |
Abstract |
The accumulation of beta amyloid (Aβ) peptides, a hallmark of Alzheimer's disease (AD) is related to mechanisms leading to neurodegeneration. Among its pleiotropic cellular effects, Aβ accumulation has been associated with a deregulation of sphingolipid metabolism. Sphingosine 1-phosphate (S1P) derived from sphingosine is emerging as a critical lipid mediator regulating various biological activities including cell proliferation, survival, migration, inflammation, or angiogenesis. S1P tissue level is low and kept under control through equilibrium between its synthesis mostly governed by sphingosine kinase-1 (SphK1) and its degradation by sphingosine 1-phosphate lyase (SPL). We have previously reported that Aβ peptides were able to decrease the activity of SphK1 in cell culture models, an effect that could be blocked by the prosurvival IGF-1/IGF-1R signaling. |
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