Display options
Cite
Cervia D, Perrotta C, Moscheni C, et al. Nitric oxide and sphingolipids control apoptosis and autophagy with a significant impact on Alzheimer's disease. J Biol Regul Homeost Agents. 2013;27(2):11-22
Cervia, D., Perrotta, C., Moscheni, C., De Palma, C., & Clementi, E. (2013). Nitric oxide and sphingolipids control apoptosis and autophagy with a significant impact on Alzheimer's disease. Journal of biological regulators and homeostatic agents, 27(2), 11-22.
Cervia, D, et al. "Nitric oxide and sphingolipids control apoptosis and autophagy with a significant impact on Alzheimer's disease." Journal of biological regulators and homeostatic agents vol. 27,2 (2013): 11-22.
Cervia D, Perrotta C, Moscheni C, De Palma C, Clementi E. Nitric oxide and sphingolipids control apoptosis and autophagy with a significant impact on Alzheimer's disease. J Biol Regul Homeost Agents. 2013 Apr-Jun;27(2):11-22. PMID: 24813312.
Copy Download .nbib Format: NLM
Share it on

J Biol Regul Homeost Agents. 2013 Apr-Jun;27(2):11-22.

Nitric oxide and sphingolipids control apoptosis and autophagy with a significant impact on Alzheimer's disease.

Journal of biological regulators and homeostatic agents

D Cervia, C Perrotta, C Moscheni, C De Palma, E Clementi

Affiliations

  1. Department for Innovation in Biological, Agro-food and Forest systems (DIBAF), Universita' della Tuscia, Viterbo, Italy.
  2. Unit of Clinical Pharmacology, National Research Council-Institute of Neuroscience, Department of Biomedical and Clinical Sciences, University Hospital L. Sacco, Universita' di Milano, Milano, Italy.
  3. Morphology Unit, Department of Biomedical and Clinical Sciences, University Hospital L. Sacco, Universita' di Milano, Milano, Italy.
  4. Unit of Clinical Pharmacology, National Research Council-Institute of Neuroscience, Department of Biomedical and Clinical Sciences, University Hospital L. Sacco, Universita? di Milano, Milano, Italy.

PMID: 24813312

Abstract

Aberrant regulation of signalling pathways promoting and regulating apoptosis and autophagy contributes to the development of most human neurodegenerative diseases characterised by progressive dysfunction and death of neuronal and glial cells. Both in central and peripheral nervous systems cell death is either apoptotic or autophagic, depending on the cellular setting and the initial pathogenic cue. While some mixed phenotypes have been reported, apoptosis and autophagy tend to develop into mutually exclusive ways to such an extent that they inhibit each other. The sphingolipid ceramide is a key intracellular signalling molecule involved in many cellular processes leading to either survival or death; in most of these processes also the short-lived gaseous messenger nitric oxide (NO) plays a crucial role. The crosstalk between these two messengers and their downstream mediators has been thus extensively investigated and we now have a deep understanding of it and of its multiple feedback controls. What we provide here are details on how NO- and sphingolipid-dependent signalling and their crosstalk impact on degenerative brain diseases, in particular Alzheimer’s disease; we also describe how the ability of these molecules to regulate autophagy and apoptosis plays a significant role in determining the pathogenic evolution of these diseases. The evidence reported in this review suggests that targeting the NO and sphingolipid-dependent signalling pathways is worth exploiting in therapeutic perspective. In order to pursue these strategies, however, we still need to understand conclusively how the crosstalk between the NO and ceramide/sphingolipid pathways balances towards beneficial vs. toxic effects. In view of the nature of the signalling pathways involved and their multiple roles, the type of crosstalk involved is complex and intermingled with other signalling pathways.

Publication Types