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Additionally, disruption of the bloodbrain barrier (BBB) occurs through endothelial injury, tight junction breakdown, and matrix metalloproteinase activation, which increases vascular permeability and contributes to cerebral edema and secondary injury (28)

These findings support the hypothesis that glycocalyx disruption contributes to the pathophysiology of DCI through mechanisms such as neuro-inflammation, microthrombosis, endothelial dysfunction, and oxidative stress (66)

The PD-1/PD-L1 pathway plays a crucial role in immune tolerance by fine-tuning the quality and duration of T cell response thereby serving as a rheostat of immune response (262, 263)