Berenson-Allen Center for Noninvasive Brain Stimulation, Division of Cognitive Neurology, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA.
Brain Topogr. 2011 Oct;24(3-4):302-15. doi: 10.1007/s10548-011-0196-8. Epub 2011 Aug 14.
Brain plasticity can be conceptualized as nature's invention to overcome limitations of the genome and adapt to a rapidly changing environment. As such, plasticity is an intrinsic property of the brain across the lifespan. However, mechanisms of plasticity may vary with age. The combination of transcranial magnetic stimulation (TMS) with electroencephalography (EEG) or functional magnetic resonance imaging (fMRI) enables clinicians and researchers to directly study local and network cortical plasticity, in humans in vivo, and characterize their changes across the age-span. Parallel, translational studies in animals can provide mechanistic insights. Here, we argue that, for each individual, the efficiency of neuronal plasticity declines throughout the age-span and may do so more or less prominently depending on variable 'starting-points' and different 'slopes of change' defined by genetic, biological, and environmental factors. Furthermore, aberrant, excessive, insufficient, or mistimed plasticity may represent the proximal pathogenic cause of neurodevelopmental and neurodegenerative disorders such as autism spectrum disorders or Alzheimer's disease.
大脑的可塑性可以被视为大自然的一种发明,旨在克服基因组的限制,以适应快速变化的环境。因此,可塑性是大脑在整个生命周期中的固有特性。然而,可塑性的机制可能会随着年龄的变化而变化。经颅磁刺激(TMS)与脑电图(EEG)或功能磁共振成像(fMRI)的结合,使临床医生和研究人员能够直接研究活体人类的局部和网络皮质可塑性,并描述其在整个年龄段的变化。在动物中的平行转化研究可以提供机制上的见解。在这里,我们认为,对于每个人来说,神经元可塑性的效率在整个年龄段内都会下降,并且可能会根据遗传、生物和环境因素定义的可变“起点”和不同的“变化斜率”,或多或少地明显下降。此外,异常、过度、不足或时机不当的可塑性可能代表自闭症谱系障碍或阿尔茨海默病等神经发育和神经退行性疾病的近端发病原因。