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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 ( 4.2 The role of neuroinflammation in AD pathogenesis Recent evidence underscores neuroinflammation as a central player in AD progression

These results collectively demonstrated the size-switchable and on-demand release behavior of the P-Mn/TI@mHSA

Once they have completed their functions and reach the end of their life span, neutrophils undergo apoptosis and then are eliminated locally by resident macrophages and dendritic cells through the process of phagocytosis [42, 51]

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