Table of Contents Author Guidelines Submit a Manuscript
Mediators of Inflammation
Volume 2017 (2017), Article ID 2470950, 8 pages
Research Article

Neutral Sphingomyelinase Behaviour in Hippocampus Neuroinflammation of MPTP-Induced Mouse Model of Parkinson’s Disease and in Embryonic Hippocampal Cells

1Department of Pharmaceutical Science, University of Perugia, Perugia, Italy
2Department of Experimental Medicine, University of Perugia, Polo Unico Sant’Andrea delle Fratte, Piazzale Gambuli, 06132 Perugia, Italy
3Inserm U 1127, CNRS UMR 7225, Sorbonne Universités, UPMC Univ Paris 06 UMR S 1127, Institut du Cerveau et de la Moelleépinière (ICM), 75013 Paris, France
4Department of Biology and Interdepartmental Research Center Nutrafood “Nutraceuticals and Food for Health”, University of Pisa, Pisa, Italy
5CRABiON-Perugia, Via Ponchielli 4, 06073 Perugia, Italy
6Department of Chemistry, Biology and Biotechnology, Via Elce di sotto, 06123 Perugia, Italy
7Dipartimento di Area Medica (DAME), University of Udine, P.le M. Kolbe 4, 33100 Udine, Italy

Correspondence should be addressed to Elisabetta Albi

Received 24 May 2017; Revised 16 September 2017; Accepted 26 September 2017; Published 16 November 2017

Academic Editor: Vinod K. Mishra

Copyright © 2017 Samuela Cataldi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Neutral sphingomyelinase is known to be implicated in growth arrest, differentiation, proliferation, and apoptosis. Although previous studies have reported the involvement of neutral sphingomyelinase in hippocampus physiopathology, its behavior in the hippocampus during Parkinson’s disease remains undetected. In this study, we show an upregulation of inducible nitric oxide synthase and a downregulation of neutral sphingomyelinase in the hippocampus of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine- (MPTP-) induced mouse model of Parkinson’s disease. Moreover, the stimulation of neutral sphingomyelinase activity with vitamin 1,25-dihydroxyvitamin D3 reduces specifically saturated fatty acid sphingomyelin by making sphingomyelin a less rigid molecule that might influence neurite plasticity. The possible biological relevance of the increase of neutral sphingomyelinase in Parkinson’s disease is discussed.