1471-4159/asset/olbannerleft.gif?v=1&s=4636ca86ad7e40d133e71d09a5d759010472e0c2)
1471-4159/asset/olbannerright.gif?v=1&s=38094197c2d87aeb3b86aa293b5858c5c15cca29)
Regulation of tyrosine kinase B activity by the Cyp46/cholesterol loss pathway in mature hippocampal neurons: relevance for neuronal survival under stress and in aging
Article first published online: 7 JAN 2011
DOI: 10.1111/j.1471-4159.2010.07079.x
© 2011 The Authors. Journal of Neurochemistry © 2011 International Society for Neurochemistry
Issue
Journal of Neurochemistry
Special Issue: Fourth ISN Special Conference 'Membrane Domains in CNS Physiology and Pathology', Erice (Trapani), Sicily, Italy, 22-26 May 2010
Volume 116, Issue 5, pages 747–755, March 2011
Additional Information
How to Cite
Sodero, A. O., Trovò, L., Iannilli, F., Van Veldhoven, P., Dotti, C. G. and Martin, M. G. (2011), Regulation of tyrosine kinase B activity by the Cyp46/cholesterol loss pathway in mature hippocampal neurons: relevance for neuronal survival under stress and in aging. Journal of Neurochemistry, 116: 747–755. doi: 10.1111/j.1471-4159.2010.07079.x
Publication History
- Issue published online: 9 FEB 2011
- Article first published online: 7 JAN 2011
- Received August 1, 2010; revised manuscript received October 17, 2010; accepted October 18, 2010.
- Abstract
- Article
- References
- Cited By
Keywords:
- aging;
- cholesterol;
- Cyp46;
- hippocampus;
- reactive oxygen species;
- tyrosine kinase B
J. Neurochem. (2011) 116, 747–755.
Abstract
It is well established that memory formation and retention involve the coordinated flow of information from the post-synaptic site of particular neuronal populations to the nucleus, where short and long-lasting modifications of gene expression occur. With age, mnemonic, motor and sensorial alterations occur, and it is believed that extra failures in the mechanisms used for memory formation and storage are the cause of neurodegenerative pathologies like Alzheimer’s disease. A prime candidate responsible for damage and loss of function during aging is the accumulation of reactive oxygen species, derived from normal oxidative metabolism. However, dysfunction in the aged brain is not paralleled by an increase in neuronal death, indicative that the brain is better suited to fight against the death signals generated from reactive oxygen species than against loss-of-function stimuli. A main aim of this laboratory is to understand how neurons perform and survive in the constitutive stress background represented by aging. In this report, we summarize our recent findings in relation to survival.