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Its inclusion in metabolic-medicine conversation reflects the growing willingness of physicians to consider mechanism-first compounds across classes

doi: 10.1093/brain/aws144 285 TzeplaeffL.WilflingS.RequardtM

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They initiate transendothelial migration by binding to intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) on cerebral endothelial cells through adhesion molecules on their surface ( Neutrophils, as the earliest infiltrating immune cells following ischemic stroke, play a critical role in exacerbating neuroinflammation and secondary brain injury through their excessive activation ( 3.2.2 Monocytes After ischemic stroke, peripheral blood monocytes are recruited to the injured brain tissue via the CCL2/CCR2 chemokine axis ( Studies have shown that the proportion of CD14++CD16+ monocytes is significantly associated with patient prognosis, making it a potential biomarker ( 3.2.3 T lymphocytes T lymphocytes exhibit complex dynamic changes and dual roles in the pathological process of ischemic stroke ( + and CD8 + T lymphocytes into the injured brain tissue is markedly increased, with a corresponding rise in the proportion of these T cell subsets ( + and CD8 + T cells persist within the central nervous system, and this sustained presence during the chronic phase may be closely associated with long-term brain injury progression and secondary neurodegeneration ( + T cells inducing direct neuronal death via the perforin-granzyme pathway ( + T cells are generally divided into T helper (Th) cells and regulatory T cells (Treg) ( + T cells participate in immune regulation after ischemic stroke through differentiation into Th1 and Th2 subsets