IMMUNE MODULATION AND ApTOLL

After a stroke, cell damage induced by the lack of blood supply causes the release of endogenous cell components to the neuron extracellular medium, triggering central nervous system alarms. One of the primary sensors of these brain damage-associated molecular patterns (DAMPs) is TLR4, a central receptor in innate immunity and expressed on the plasmatic membrane of immune cells such as microglia, neutrophils, monocytes, macrophages, among others. TLR4’s activation initiates a cascade of triggers that ultimately leads to the production and release of pro-inflammatory mediators, causing uncontrolled inflammation, further cell damage, and subsequent worsening of the brain lesion. ApTOLL has a powerful immunomodulatory effect through antagonistic action on TLR4 receptors, inhibiting the inflammatory cascade.
ApTOLL’s anti-inflammatory effect has been linked with a high level of brain protection, reducing infarct volume up to 65% in preclinical studies. Aptamers’ mode of action and short half-life matches perfectly with the ideal time-frame to modulate inflammation and while minimizing the side effects.

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