Chondroitinase treatment

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Chondroitinase treatment
Specialty Neurology

Chondroitinase treatment is a treatment of proteoglycans, a protein in the fluid among cells where they affect neural communication, plasticity, and other things. [1] Chondroitinase treatment has been shown to allow adults' vision to be restored as far as ocular dominance is concerned. [2] Moreover, there is some evidence that chondroitinase could treat spinal injuries. [3]

The enzyme chondroitinase ABC is used in this treatment and derives from the bacterium Proteus vulgaris. [4] In 2018, pre-clinical research involving the chondroitinase ABC enzyme has been mainly directed towards treating spinal cord injuries in test animals using viral vectors. [5] In general, chondroitinase ABC works in vivo by cleaving off the side chains of chondroitin sulfate proteoglycans (CSPGs), which are over-produced by glial cells in the central nervous system when a spinal injury occurs. [4] [5] Chondroitin sulfate proteoglycans bonded to their side chains called chondroitin sulfate glycosaminoglycans prevent neuroregeneration in the central nervous system by forming glial scar tissue, which inhibits both neuroplasticity and repair of damaged axons. [5] [6] However, when the side chains of the chondroitin sulfate proteoglycans are cleaved by chondroitinase ABC, this promotes the damaged region of the CNS to recover from the spinal cord injury. [4]

A 2020 study proposed that chondroitinase treatment promotes plasticity by activating tropomyosin receptor kinase B—receptor for brain-derived neurotrophic factor and a major plasticity orchestrator in the brain. [7] Cleavage of CSPGs by chondroitinase ABC leads to inactivation of PTPRS, the membrane receptor for CSPGs and a phosphatase that inactivates TRKB under normal physiological conditions, which subsequently promotes TRKB phosphorylation and activation of neuroplasticity.[ citation needed ]

See also

References

  1. ↑ Cambridge Centre for Brain Repair, School of Clinical Medicine, Cambridge Centre for Brain Repair. Plasticity and the extracellular matrix. Archived 2007-12-03 at the Wayback Machine
  2. ↑ Hensch TK (2005). "Critical period mechanisms in developing visual cortex". Neural Development. Current Topics in Developmental Biology. Vol. 69. pp. 215–37. doi:10.1016/S0070-2153(05)69008-4. ISBN   9780121531690. PMID   16243601.
  3. ↑ "Spinal injury regeneration hope". BBC NEWS, online. 17 February 2008. Retrieved 2009-12-31.
  4. 1 2 3 Zhao RR, Fawcett JW (August 2013). "Combination treatment with chondroitinase ABC in spinal cord injury--breaking the barrier". Neuroscience Bulletin. 29 (4): 477–83. doi:10.1007/s12264-013-1359-2. PMC   5561941 . PMID   23839053.
  5. 1 2 3 Burnside ER, De Winter F, Didangelos A, James ND, Andreica EC, Layard-Horsfall H, Muir EM, Verhaagen J, Bradbury EJ (August 2018). "Immune-evasive gene switch enables regulated delivery of chondroitinase after spinal cord injury". Brain. 141 (8): 2362–2381. doi:10.1093/brain/awy158. PMC   6061881 . PMID   29912283.
  6. ↑ Bradbury EJ, Carter LM (March 2011). "Manipulating the glial scar: chondroitinase ABC as a therapy for spinal cord injury". Brain Research Bulletin. 84 (4–5): 306–16. doi:10.1016/j.brainresbull.2010.06.015. PMID   20620201. S2CID   10605553.
  7. ↑ Lesnikova, Angelina; Casarotto, Plinio Cabrera; Fred, Senem Merve; Voipio, Mikko; Winkel, Frederike; Steinzeig, Anna; Antila, Hanna; Umemori, Juzoh; Biojone, Caroline; Castrén, Eero (2020-12-08). "Chondroitinase and antidepressants promote plasticity by releasing TRKB from dephosphorylating control of PTPσ in parvalbumin neurons". Journal of Neuroscience. 41 (5): 972–980. doi: 10.1523/JNEUROSCI.2228-20.2020 . ISSN   0270-6474. PMC   7880295 . PMID   33293360.
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