Recent publications report that although the mitochondria population in an axon can be quickly replaced by a combination of retrograde and anterograde axonal transport (often within less than 24 hours), the axon contains much older mitochondria. This suggests that not all mitochondria that reach the soma are degraded and that some are recirculating back into the axon. To explain this, we developed a model that simulates mitochondria distribution when a portion of mitochondria that return to the soma are redirected back to the axon rather than being destroyed in somatic lysosomes. Utilizing the developed model, we studied how the percentage of returning mitochondria affects the mean age and age density distributions of mitochondria at different distances from the soma. We also investigated whether turning off the mitochondrial anchoring switch can reduce the mean age of mitochondria. For this purpose, we studied the effect of reducing the value of a parameter that characterizes the probability of mitochondria transition to the stationary (anchored) state. The reduction in mitochondria mean age observed when the anchoring probability is reduced suggests that some injured neurons may be saved if the percentage of stationary mitochondria is decreased. The replacement of possibly damaged stationary mitochondria with newly synthesized ones may restore the energy supply in an injured axon. We also performed a sensitivity study of the mean age of stationary mitochondria to the parameter that determines what portion of mitochondria re-enter the axon and the parameter that determines the probability of mitochondria transition to the stationary state. The sensitivity of the mean age of stationary mitochondria to the mitochondria stopping probability increases linearly with the number of compartments in the axon. High stopping probability in long axons can significantly increase mitochondrial age.

中文翻译：

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线粒体循环对线粒体年龄密度分布的影响


最近的出版物报告称，尽管轴突中的线粒体群可以通过逆行和顺行轴突运输的组合（通常在不到 24 小时内）快速替换，但轴突中含有更古老的线粒体。这表明并非所有到达体细胞的线粒体都会被降解，有些线粒体会再循环回轴突。为了解释这一点，我们开发了一个模型，模拟当返回体细胞的线粒体的一部分被重定向回轴突而不是在体细胞溶酶体中被破坏时线粒体的分布。利用开发的模型，我们研究了返回线粒体的百分比如何影响距体体不同距离处线粒体的平均年龄和年龄密度分布。我们还研究了关闭线粒体锚定开关是否可以降低线粒体的平均年龄。为此，我们研究了降低表征线粒体过渡到静止（锚定）状态概率的参数值的影响。当锚定概率降低时观察到的线粒体平均年龄的降低表明，如果静止线粒体的百分比降低，一些受伤的神经元可能会得到挽救。用新合成的线粒体替换可能受损的静止线粒体可能会恢复受损轴突的能量供应。我们还对静止线粒体的平均年龄对确定线粒体的哪一部分重新进入轴突的参数以及确定线粒体转变为静止状态的概率的参数进行了敏感性研究。 静止线粒体的平均年龄对线粒体停止概率的敏感性随着轴突中的隔室数量线性增加。长轴突的高停止概率会显着增加线粒体年龄。