PET tracers targeting pathophysiological mechanisms of ischemic stroke: A comprehensive review

Ischemic stroke remains a major cause of disability and mortality worldwide. The underlying pathophysiological mechanisms are intricate, involving multiple aspects such as inadequate cerebral perfusion, metabolic disturbances, neuroinflammatory responses, disruption of the blood-brain barrier, and accumulation of pathological proteins. Positron emission tomography (PET), a non-invasive imaging modality, has emerged as a crucial tool for investigating the mechanisms underlying ischemic stroke, facilitating early diagnosis, evaluating treatment efficacy, and monitoring prognosis by employing radiotracers that target diverse pathological processes. This review summarizes recent advancements in the application of PET radiotracers for the investigation of various pathological mechanisms associated with ischemic stroke, including cerebral perfusion and hypoxia (such as 15 O-H 2 O), glucose metabolism (such as 18 F- fluorodeoxyglucose [FDG]), neuroinflammation (such as 18 F-GE-180), vascular permeability (such as 18 F-BR-351), as well as the presence of β-amyloid and tau (such as 11 C-PiB, 18 F-MK-6240). Studies indicate that these radiotracers can effectively reflect the dynamic processes of brain injury and repair in both preclinical models and clinical settings, elucidating critical molecular events in disease progression and offering novel perspectives for individualized therapeutic strategies. Future investigations should focus on improving the pharmacological properties of these radiotracers and exploring the synergistic application of multimodal imaging techniques to advance precision medicine in the context of ischemic stroke.