Biomedical Engineering Reference
In-Depth Information
Lesion
cavity
Proteoglycan
upregulation (Glial scar)
Inflammatory cell
Reactive astrocyte
Dystrophic
neurons
Secondary
axon damage
Dying neuron
Axon
sprouting
Axon demyelination
Figure 6.3 Schematic diagram of the processes of wounding
healing, secondary damage, and abortive regeneration in the
CNS. Reproduced with permission from M.T. Fitch and J. Silver,
Experimental Neurology , 2008, 209 , 2, 294. ©2008, Elsevier [16]
The regenerative capacity of damaged brain tissue is greatly inhibited
by the growth inhibitory environment around the lesion cavity [18],
which is mainly attributed to the following reasons: (1) mature
neurons lose their self-renewal capacity and exist in a non-dividing
state; (2) an influx of inflammatory cells and reactive astrocytes
lead to the formation of a glial scar that forms a mechanical barrier
and causes the secondary damage to regrown axons; (3) reactive
astrocytes up-regulate inhibitory molecules such as chondroitin
sulfate proteoglycans; (4) some myelin-associated proteins, including
myelin-associated glycoproterin (MAG), oligodendrocyte-myelin
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