In recent years, the role of lactate metabolism and its derived lactylation modifications in Alzheimer's disease has received increasing attention. Studies have shown that in the brains of Alzheimer's disease patients, glucose metabolism is significantly reduced, while glycolysis is upregulated, and lactate levels are elevated. Nevertheless, the research regarding the relationship between lactylation and Alzheimer's disease remains limited. Building on recent advances in understanding lactylation in neurodegenerative diseases and related conditions, the authors analyze and explore the potential relationships between lactylation and Alzheimer's disease from the perspectives of -amyloid deposition, tau protein pathology, and neuroinflammation. In summary, lactylation, as a novel post-translational modification holds significant promise in elucidating the pathological mechanisms and advancing the treatment of Alzheimer's disease. A deeper investigation into its molecular mechanisms and regulatory networks may open new avenues for the diagnosis and treatment of Alzheimer's disease.

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The authors' purpose was to develop and validate a predictive model for futile recanalization after EVT by integrating arterial-venous collateral assessment with clinical parameters. Patients were stratified into training, internal validation, and completely independent external validation cohorts collected from a separate medical center. Three independent predictors were identified: age, whole-brain arterial collateral status, and whole-brain venous collateral status. The model demonstrated excellent discrimination in the training cohort, internal validation cohort, and notably maintained robust performance in the completely independent external validation cohort. The integration of whole-brain arterial-venous collateral assessment with clinical parameters shows potential value in predicting futile recanalization after EVT. This model, validated across multiple cohorts, may provide additional information to support clinical decision-making.

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