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

J. Neurochem. (2011) 116, 747–755. 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, mnem...

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Published in:Journal of neurochemistry 2011-03, Vol.116 (5), p.747-755
Main Authors: Sodero, Alejandro O., Trovò, Laura, Iannilli, Francesca, Van Veldhoven, Paul, Dotti, Carlos G., Martin, Mauricio G.
Format: Article
Language:English
Subjects:
Aging
Alzheimer's disease
Animals
Brain
Brain research
Cell Death - physiology
Cell survival
Cholesterol
Cholesterol - metabolism
Cholesterol 24-Hydroxylase
Cyp46
Gene expression
Hippocampus
Hippocampus - cytology
Hippocampus - enzymology
Humans
Kinases
Memory
Models, Biological
Neurochemistry
Neurodegenerative diseases
Neurons
Neurons - enzymology
Oxidative metabolism
Oxidative Stress - physiology
Protein-tyrosine kinase
Protein-Tyrosine Kinases - metabolism
Reactive oxygen species
Reviews
Signal Transduction - physiology
Steroid Hydroxylases - metabolism
Stress
Stress, Physiological - physiology
tyrosine kinase B
Up-Regulation - physiology
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Summary:J. Neurochem. (2011) 116, 747–755. 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.
ISSN:0022-3042
1471-4159
DOI:10.1111/j.1471-4159.2010.07079.x