Kovacic Uros, Sketelj Janez, Bajrović Fajko F
Institute of Pathophysiology, Faculty of Medicine, University of Ljubljana, SI-1000 Ljubljana, Slovenia.
Int Rev Neurobiol. 2009;87:465-82. doi: 10.1016/S0074-7742(09)87026-8.
Numerous and extensive functional, structural, and biochemical changes characterize intact aged peripheral nervous system. Functional recovery after peripheral nerve injury depends on survival of injured neurons and functional reinnervation of target tissue by regeneration of injured axons and collateral sprouting of uninjured (intact) adjacent axons. The rate of axonal regeneration becomes slower and its extent (density and number of regenerating axons) decreases in aged animals. Aging also impairs terminal sprouting of regenerated axons and collateral sprouting of intact adjacent axons, thus further limiting target reinnervation and its functional recovery. Decreased survival of aged noninjured and injured neurons, limited intrinsic growth potential of neuron, alteration in its responsiveness to stimulatory or inhibitory environmental factors, and changes in the peripheral neural pathways and target tissues are possible reasons for impaired reinnervation after peripheral nerve injury in old age. The review of present data suggests that this impairment is mostly due to the age-related changes in the peripheral neural pathways and target tissues, and not due to the limited intrinsic growth capacity of neurons or their reduced responsiveness to trophic factors. Age-related alterations in the soluble target derived neurotrophic factors, like nerve growth factor, and nonsoluble extracellular matrix components of neural pathways, like laminin, might be important in this respect.
完整的老年外周神经系统具有众多广泛的功能、结构和生化变化。外周神经损伤后的功能恢复取决于受损神经元的存活以及受损轴突的再生和未受损（完整）相邻轴突的侧支发芽对靶组织的功能性再支配。在老年动物中，轴突再生速度变慢，其程度（再生轴突的密度和数量）降低。衰老还会损害再生轴突的终末发芽和完整相邻轴突的侧支发芽，从而进一步限制靶组织的再支配及其功能恢复。老年未受损和受损神经元的存活率降低、神经元内在生长潜力有限、其对刺激性或抑制性环境因素的反应性改变以及外周神经通路和靶组织的变化，可能是老年外周神经损伤后再支配受损的原因。对现有数据的综述表明，这种损伤主要是由于外周神经通路和靶组织的年龄相关变化，而不是由于神经元内在生长能力有限或它们对神经营养因子的反应性降低。在这方面，可溶性靶源性神经营养因子（如神经生长因子）和神经通路的不溶性细胞外基质成分（如层粘连蛋白）的年龄相关改变可能很重要。
