Axon Regeneration in the Peripheral and Central Nervous Systems

Results Probl Cell Differ, 2009 · DOI: 10.1007/400_2009_19 · Published: January 1, 2009

Simple Explanation

In the mature mammalian central nervous system (CNS), axon regeneration is very limited after injury, leading to persistent functional deficits. This contrasts with the peripheral nervous system (PNS), where axons can regenerate over long distances, allowing for substantial functional recovery in adults. Both extracellular molecules and the neuron's intrinsic growth capacity play roles in determining the success of axon regeneration.

Study Duration

Not specified

Participants

Not specified

Evidence Level

Review

Key Findings

1
The PNS environment is stimulatory and/or the CNS environment is inhibitory for axon growth.
2
Inhibitors of regeneration include specific proteins in CNS myelin and molecules associated with the astroglial scar.
3
CNS neurons do not upregulate growth-associated genes to the same extent as do PNS neurons.

Research Summary

Axon regeneration in the mature mammalian central nervous system (CNS) is extremely limited after injury. This situation differs from that in the mammalian peripheral nervous system (PNS), where long- distance axon regeneration and substantial functional recovery can occur in the adult. Both extracellular molecules and the intrinsic growth capacity of the neuron influence regenerative success.

Practical Implications

Therapeutic Development

Understanding factors influencing axon growth is crucial for developing therapeutics to promote CNS regeneration.

Targeted Interventions

Targeting myelin-associated inhibitors (MAIs) and chondroitin sulfate proteoglycans (CSPGs) can promote axon regeneration in the CNS.

Enhancing Intrinsic Growth

Increasing the intrinsic growth capacity of neurons can allow for modest axon regeneration within the CNS.

Study Limitations

1
CNS regeneration studies do not always distinguish between regeneration, sprouting and synaptic plasticity.
2
Replacement of lost neuronal cell bodies, a prominent component of many CNS disorders, is beyond the scope of this chapter.
3
Phenotype of Nogo-A deletion is modulated by strain background, age and axonal tract.

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