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The growing understanding of AD as a multifactorial disease necessitates an approach that simultaneously addresses tau pathology, neuroinflammation, oxidative stress, mitochondrial dysfunction, and synaptic loss (Chu et al., 2024)

Received 03 December 2023

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Initially, 22.52P meshes exhibited acute inflammation and upregulated expression of monocyte (CD68) and myeloid lineage genes (Cd11b)