Chondroitinase treatment is a treatment of proteoglycans, a protein in the fluid among cells where (among other things) they affect neural activity (communication, plasticity).[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 be used for the treatment of spinal injuries.[3]
| Chondroitinase treatment | |
|---|---|
| Specialty | neurology |
In addition, the enzyme that is used in the chondroitinase treatment, chondroitinase ABC, derives from the bacterium Proteus vulgaris.[4] In recent years, pre-clinical research involving the chondroitinase ABC enzyme has been mainly directed towards utilizing it as a way of treating spinal cord injuries in test animals using viral vectors.[5] In general, the way chondroitinase ABC works in vivo is it cleaves off the side chains of molecules known as chondroitin sulfate proteoglycans (CSPGs) which are over produced by glial cells in the central nervous system when a spinal injury occurs.[4][5] When chondroitin sulfate proteoglycans are bonded to their side chains called chondroitin sulfate glycosaminoglycans, these molecules are known to prevent neural restoration to the damaged region of the central nervous system because they form 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]
It has recently been proposed that chondroitinase treatment promotes plasticity by activation of 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 edit
References edit
- ^ 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
- ^ 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.
- ^ "Spinal injury regeneration hope". BBC NEWS, online. 17 February 2008. Retrieved 2009-12-31.
- ^ a b c 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.
- ^ a b c 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.
- ^ 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.
- ^ 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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