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  4. Cathepsins in neuronal plasticity

Cathepsins in neuronal plasticity

Neural Regen Res, 2021 · DOI: https://doi.org/10.4103/1673-5374.286948 · Published: January 1, 2021

Spinal Cord InjuryNeurologyNeuroplasticity

Simple Explanation

Proteases are enzymes that break down other proteins. Cathepsins are a class of proteases found in lysosomes, which are important for cellular degradation and recycling. Cathepsins are involved in many cell activities; this review focuses on their role in neuronal plasticity, especially Cathepsin B. Cathepsin activity is essential for lysosomes to function. When lysosomes don't work correctly, cellular processes are disrupted. However, controlled activation of cathepsins in specific neuronal structures, like growth cones and dendritic spines, aids in their plasticity. This review looks at how cathepsin activity is regulated and what happens when it's not. It clarifies how cathepsins can contribute to both neuronal plasticity and neurodegeneration.

Study Duration
Not specified
Participants
Not specified
Evidence Level
Review

Key Findings

  • 1
    Dysregulation of cathepsins, particularly after spinal cord injury, exacerbates inflammation and damages tissue, disrupting processes like autophagy and lysosomal function.
  • 2
    Cathepsins B and D are involved in extracellular matrix remodeling, which is important for neuronal plasticity, including axon regeneration and dendritic spine growth in the central nervous system.
  • 3
    Cathepsin B secretion by axon growth cones is crucial for remodeling the extracellular matrix and degrading regeneration-inhibitory CSPGs after spinal cord injury. Understanding the role of cathepsin B will help enhance neuronal plasticity.

Research Summary

Cathepsins are proteases vital for lysosomal function and involved in neuronal plasticity. Their activity must be tightly regulated to prevent detrimental effects. Following spinal cord injury, cathepsin dysregulation exacerbates inflammation and perturbs cellular processes. However, controlled cathepsin activity is crucial for extracellular matrix remodeling and neuronal plasticity. Cathepsins affect axon outgrowth by promoting axonal homeostasis and degrading inhibitory extracellular matrix constituents. They also play a role in synaptic plasticity by influencing dendritic spine growth and synaptogenesis.

Practical Implications

Therapeutic Potential

Harnessing cathepsin activity in specific cell types could enhance neuronal plasticity after trauma or disease.

Understanding Neurodegeneration

Investigating the role of cathepsins in neurodegenerative diseases may reveal new therapeutic targets.

Targeted Drug Delivery

Developing methods for controlled cathepsin secretion could promote axon regeneration and synaptic plasticity.

Study Limitations

  • 1
    The review primarily focuses on Cathepsin B, potentially overlooking the roles of other cathepsins.
  • 2
    The exact mechanisms by which cathepsins are regulated and dysregulated after spinal cord injury are still not completely understood.
  • 3
    Further research is needed to fully elucidate the link between lysosomal-autophagic flux, CSPGs, and axon inhibition.

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