Other suggestive information has been derived from the FPA and Fbg signals. Recently, the implication of Fbg and its fragments which leaked from the plasma through blood-brain barrier disruption has assumed a more complex profile during the pathogenic cascade of MS, not only for the chemoattractant action towards neutrophils, monocytes and macrophages in the inflammatory phase, but also as an early trigger of microglial activation that leads to the axonal damage. Fbg appeared to be a determinant factor in the release of oxygen reactive species in microglial cells via the protein interaction with the CD11b/ CD18 integrin receptor, a Colistin Sulfate crucial step in the mechanism of axonal damage that may be inhibited by anticoagulant drugs. Fibrin deposits were also described in chronic progressive MS plaques, whereas a MALDI-TOF spectrometry analysis revealed the downregulation of its signal in PPMS subjects. With caution due to the low number of subjects, we hypothesized that the upregulation of Fbg and FPA observed in our PrMS sample might be considered a marker of the progression onset. In support of this hypothesis, the intensities of both proteins significantly correlated with the baseline disability score. One possible explanation might be that these proteins gradually increase during the MS course, and when their levels reach a given threshold, they Acetylcorynoline accumulate in a ����toxic���� concentration for microglia and oligodendrocytes, thus reinforcing the axonal damage. However, further studies need to be performed in order to confirm this hypothesis. Few notes on Tb4, a protein highly expressed in oligodendrocytes and correlated with cellular growth and regeneration mainly by modulating the availability of cellular actin monomers. Its function remains controversial; Morris et al demonstrated that the administration of Tb4 ameliorated EAE by exerting antiinflammatory properties, and clinical improvements were also observed after the same treatment in case of stroke and brain injury, in support of its role in cellular plasticity.Conversely, silencing the Tb4 gene reduced the invasiveness of the tumor cells in glioblastoma.