Moreover, the modulation of neuroinflammation through CD22 has shown promise in alleviating Aβ-induced inflammatory responses in microglia, highlighting potential therapeutic avenues for AD (ref: Mai doi.org/10.1186/s12974-025-03361-2/). Interestingly, sex-specific influences of the APOEε4 genotype on neurogenesis have been observed, with male carriers exhibiting reduced neural progenitor cells and increased microglial presence compared to their wildtype counterparts, while female carriers showed enhanced neurogenesis (ref: Lee doi.org/10.1186/s13293-025-00694-8/). These findings underscore the importance of understanding microglial dynamics and their metabolic states in the context of AD, as they may reveal novel targets for intervention and therapeutic strategies.

The cytosolic DNA sensing pathway involving cGAS has also been implicated in AD pathogenesis, with its deletion preserving intercellular communication and alleviating Aβ-induced pathogenesis (ref: He doi.org/10.1002/advs.202410910/). Furthermore, elevated plasma levels of soluble TREM2 have been associated with cognitive decline and mortality in chronic heart failure patients, indicating a potential link between systemic inflammation and neurodegenerative processes (ref: Traub doi.org/10.1152/ajpheart.00728.2024/). These findings collectively emphasize the intricate relationship between inflammation, immune responses, and the progression of Alzheimer's disease, highlighting the need for targeted therapeutic strategies.

Moreover, the therapeutic potential of Tetrahydroxy Stilbene Glycoside (TSG) has been explored, demonstrating its ability to modulate microglial activation through the TREM2/PI3K/AKT signaling pathway, thereby reducing Aβ deposition in AD models (ref: Li doi.org/10.1111/bcpt.70008/). These findings highlight the importance of understanding microglial metabolism and lipid handling as potential therapeutic targets for Alzheimer's disease, suggesting that interventions aimed at modulating these processes could enhance microglial function and mitigate disease progression.

Furthermore, the role of soluble TREM2 in cognitive decline has been explored, with elevated plasma levels correlating with cognitive impairment in chronic heart failure patients, suggesting a systemic inflammatory component to neurodegeneration (ref: Traub doi.org/10.1152/ajpheart.00728.2024/). These findings underscore the complex interplay between neuroinflammation and cognitive function in Alzheimer's disease, emphasizing the need for therapeutic strategies that target inflammatory pathways to mitigate cognitive decline.

Moreover, the anti-inflammatory effects of Sclareol have been evaluated, revealing its ability to inhibit microglial inflammation through interactions with CDK9, thereby improving AD pathology (ref: Tang doi.org/10.1016/j.phymed.2025.156504/). These findings highlight the potential of targeting microglial pathways as a therapeutic approach in Alzheimer's disease, suggesting that interventions aimed at modulating microglial activation and function could lead to improved clinical outcomes.

Furthermore, the role of sex-specific genetic factors, such as the APOEε4 genotype, has been explored, revealing differences in neurogenesis and microglial activation between male and female carriers (ref: Lee doi.org/10.1186/s13293-025-00694-8/). The involvement of TREM2 in modulating inflammation and lipid metabolism further emphasizes the complexity of molecular interactions in AD (ref: Traub doi.org/10.1152/ajpheart.00728.2024/). These insights into the molecular mechanisms of Alzheimer's disease provide a foundation for targeted therapeutic strategies aimed at mitigating disease progression.

Moreover, the role of methionine aminopeptidase 2 (MetAP2) inhibitors in modulating inflammation in microglia suggests that epigenetic regulation may also influence neuroinflammatory responses in AD (ref: Zhang doi.org/10.3390/molecules30030620/). These findings highlight the importance of understanding genetic and epigenetic factors in Alzheimer's disease, as they may provide insights into personalized therapeutic approaches and the development of targeted interventions.

Furthermore, the accumulation of microplastics has been linked to increased neuroinflammation and neuronal death following cerebral ischemia, raising concerns about environmental pollutants and their impact on brain health (ref: Kim doi.org/10.3390/cells14040241/). These findings underscore the importance of considering environmental and lifestyle factors in the context of Alzheimer's disease, as they may contribute to disease risk and progression, highlighting the need for preventive strategies that address these influences.