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The mechanisms of TB-500 are still being investigated, but known actions of TB4 include: Binding as an actin-binding protein to inhibit the polymerization of globular actin (G-actin) into filamentous actin (F-actin), known as actin sequestration, which results in higher G-actin levels and increased cellular motility [23, 24] TB4s ability to increase cellular motility may help progenitor cells to reach sites of injury and initiate tissue recovery [25]
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Individual consent was not necessary due to the retrospective design of the study
Dandy-Walker complex and other CNS structural abnormalities, such as posterior fossae cysts, syringomyelia, arachnoid cysts, intraspinal lipomas, and defects of the vertebrae or skull have been described in patients with NCM and likely portend a greater likelihood of developing symptomatic NCM
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