Table 1.

Synoptic view of main features of acute and chronic CNS fibro-glial scar.

CNS disease	Responder cells	Mediators	ECM component
Acute damage	Astrocytes, microglia, leukocytes, meningeal cells, fibroblasts, pericytes	Thrombin, MMP-9, ATP, PDGFRβ, TGFβ	Fibronectin, laminin, collagen, CSPGs, tenascin, HSPGs
ALS	Astrocytes, microglia, leukocytes, oligodendrocytes, meningeal cells, fibroblasts, pericytes	IL-6, CXCL1, CXCL10, CXCL12, TNFα, TGFβ, NGF, INFγ, PGD2, ADAMTS-4, CTGF, S100A4, MMP-9	Fibronectin, collagen IV, CSPGs, Sema3A, fibrin, vimentin, thrombin
MS	Astrocytes, microglia, leukocytes, endothelial cells, meningeal cells, fibroblasts, pericytes, oligodendrocytes	PDGFRβ, TGFβ, myelin	Collagen, fibronectin, biglycan, decorin, CSPGs
AD	Astrocytes, microglia, leukocytes, smooth muscle cells, fibroblasts, pericytes	PDGFRβ, TGFβ	GAGs, HSPGs

The table summarizes the main cellular components, mediators and ECM molecules involved in ALS, MS, and AD as well as in acute CNS damage. For a more extensive review of the many specific molecules that regulate or influence CNS cellular responses to acute conditions see (3, 4). CTGF, connective tissue growth factor; INFγ, interferon γ; MMP-9, matrix metalloprotease-9; NGF, nerve growth factor; PGD2, prostaglandin D2; TNFα, tumor necrosis factor α.