期刊
JOURNAL OF NEUROCHEMISTRY
卷 116, 期 5, 页码 747-755出版社
WILEY
DOI: 10.1111/j.1471-4159.2010.07079.x
关键词
aging; cholesterol; Cyp46; hippocampus; reactive oxygen species; tyrosine kinase B
资金
- Fund for Scientific Research Flanders (FWO)
- Federal Office for Scientific Affairs [IUAP P6/43]
- SAO-FRMA Grant
- Flemish Government
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.
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