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Owing to their diverse etiologies, onset ages, and potential repair mechanisms, the discovery of new treatments for treating myelin pathologies should aim at globally stimulating endogenous oligodendrogenesis, known to spontaneously increase following injury, at multiple levels, i.e., from the specification of new OPCs from neural progenitor cells (NPCs), to the maturation of pre-existing ones within the parenchyma

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Here we demonstrate that deletion of rv1127c results in dysregulated CCM, disruption in both redox balance and in bioenergetics, when grown on propionate-containing, or yielding medium, and reduced survival and virulence of Mtb in two different murine models of TB

While their mechanisms may differ, their combination has been proposed to provide complementary or synergistic actions