Key result
APOE genetic polymorphisms influence ischemic stroke incidence, severity, functional recovery, and associated cognitive dysfunction.
Why the study?
Stroke is a leading cause of mortality and disability, and APOE genetic polymorphisms influence ischemic stroke incidence, severity, functional recovery, and cognitive dysfunction.
Understanding the role of APOE genetic polymorphisms in ischemic stroke may offer valuable perspectives for identifying risk factors and developing targeted therapeutic strategies.
APOE polymorphisms may influence IS recovery; leaves open targeted interventions pending prospective human trials.
Stroke remains a leading cause of mortality and disability, presenting a substantial public health challenge. In China, millions of individuals are affected by stroke, with an increasing prevalence among younger populations, exacerbating socioeconomic burdens. Ischemic stroke (IS), accounting for over 80% of all stroke cases, is primarily caused by cerebral artery occlusion, leading to brain tissue ischemia and subsequent neurological deficits. Apolipoprotein E (APOE), a key regulator of lipid metabolism and vascular function, plays a critical role in IS pathogenesis and recovery. Recent studies have highlighted the influence of APOE genetic polymorphisms on stroke incidence, severity, functional recovery, and associated cognitive dysfunction. Additionally, animal models provide insights into the molecular mechanisms of APOE in ischemic brain injury and repair. This review summarizes the latest findings on the role of APOE in IS, encompassing its impact on stroke prevalence, recovery, cognitive outcomes, and related conditions. These insights may offer valuable perspectives for identifying risk factors and developing targeted therapeutic strategies for IS.
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Yuan et al. (2025) conducted a review in Ischemic stroke. APOE genetic polymorphisms was evaluated. APOE genetic polymorphisms influence ischemic stroke incidence, severity, functional recovery, and associated cognitive dysfunction.
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