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The mechanism may be related to increasing the content of inhibitory amino acids and their receptor expression in rats with spastic paralysis after stroke, thereby enhancing the signal transduction of inhibitory amino acids

thaliana auxin biosynthetic gene AtYUC8 and AtACS8 , thereby fine-tuning the auxin-ethylene balance and reducing ethylene biosynthesis

In vitro BBB models further show that oligomeric -syn specifically (not monomeric or fibrillar species) disrupts BBB integrity through astrocyte-dependent mechanisms, implicating pathogenic neuronal -syn species as key upstream initiators of vascular fluctuations ( Neuronal -syn pathology drives astrocyte activation through possible release of inflammatory and oxidative stress signals and exposure to extracellular oligomeric species, triggering NF-Bdependent transcription, cytokine production, and in some cases inflammatory senescence (Sorrentino et al., 2017, 2020)