Plasticity and injury in the developing brain.
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.
Johnston
Michael V
MV
Department of Neurology, Kennedy Krieger Institute and Johns Hopkins University, School of Medicine, 707 North Broadway, Baltimore, MD 21205, USA. Johnston@kennedykrieger.org
Ishida
Akira
A
Ishida
Wako Nakajima
WN
Matsushita
Hiroko Baber
HB
Nishimura
Akira
A
Tsuji
Masahiro
M
D001921:Brain / Q000473:pathology / Q000503:physiopathology*; D001930:Brain Injuries / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D002648:Child; D005600:Fragile X Syndrome / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D006801:Humans; D020925:Hypoxia-Ischemia, Brain / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D008607:Intellectual Disability / Q000473:pathology / Q000503:physiopathology*; D009473:Neuronal Plasticity; D015518:Rett Syndrome / Q000473:pathology / Q000503:physiopathology / Q000628:therapy