They are known to be structural components of a variety of human tissues, including cartilage, and also play key roles in neural development and glial scar formation.
Each GAG chain consists of a linear pattern of alternating monosaccharide units: uronic acid and either N-acetylglucosamine or N-acetylgalactosamine.
[1] The following CSPGs have been identified: Neurocan, brevican, versican, and aggrecan all share similar N-terminal and C-terminal domains.
[2] CSPGs guide growth cones through the use of negative signals, as seen by the fact that growing axons avoid CSPG dense areas.
[4] These results suggest that CSPGs act in neural development as an inhibitory signal to help guide growing axons.
[5] CSPGs are known to be part of the glial scar that forms post injury, acting as a barrier to prevent axon extension and regrowth.
PTP-sigma (a transmembrane protein tyrosine phosphatase) is a recently discovered receptor for CSPGs, and is important for proper CSPG function.
[8] To simulate more physiological situations, researchers looked at PTP-sigma effects on spinal cord injury sites in mice.
Mice with induced spinal cord injury lacking PTP-sigma showed significantly more axon regrowth, with normal amounts of CSPG present.
[9] The CSPG inhibition of axon regrowth and neurogenesis post spinal cord injury has been shown to be associated with the rho-associated protein kinase (ROCK) pathway.
[6] However, using C3 transferase and Y27632, two inhibitors of the ROCK signaling pathway, researchers showed that neurogenesis and new neuron length both significantly increased.
Studies have shown that CSPGs are present in the frontal cortex and hippocampus NFTs and SPs of postmortem brains of Alzheimer's patients.
[11] Research has shown a decrease in phosphacan in both the temporal lobe and the hippocampus in epilepsy cases, suggesting that there CSPGs play a role in the control of axonal regrowth.