| Literature DB >> 18490122 |
Michael V Johnston1, Akira Ishida, Wako Nakajima Ishida, Hiroko Baber Matsushita, Akira Nishimura, Masahiro Tsuji.
Abstract
The child's brain is more malleable or plastic than that of adults and this accounts for the ability of children to learn new skills quickly or recovery from brain injuries. Several mechanisms contribute to this ability including overproduction and deletion of neurons and synapses, and activity-dependent stabilization of synapses. The molecular mechanisms for activity-dependent synaptic plasticity are being discovered and this is leading to a better understanding of the pathogenesis of several disorders including neurofibromatosis, tuberous sclerosis, Fragile X syndrome and Rett syndrome. Many of the same pathways involved in synaptic plasticity, such as glutamate-mediated excitation, can also mediate brain injury when the brain is exposed to stress or energy failure such as hypoxia-ischemia. Recent evidence indicates that cell death pathways activated by injury differ between males and females. This new information about the molecular pathways involved in brain plasticity and injury are leading to insights that will provide better therapies for pediatric neurological disorders.Entities:
Mesh:
Year: 2008 PMID: 18490122 PMCID: PMC2660856 DOI: 10.1016/j.braindev.2008.03.014
Source DB: PubMed Journal: Brain Dev ISSN: 0387-7604 Impact factor: 1.961