Alzheimer's disease (AD) represents a significant and growing global health challenge, characterized by progressive cognitive decline and neurodegeneration. While the accumulation of amyloid-beta (Aβ) plaques and neurofibrillary tangles of tau protein have long been considered the primary pathological hallmarks of AD, an increasing body of evidence highlights the critical role of neuroinflammation in the disease's onset and progression. Recent approvals of Aβ-targeting therapies like lecanemab and donanemab underscore the importance of pathways regulating Aβ accumulation, where neuroinflammation plays a significant part. These advancements indirectly emphasize the interconnectedness of amyloid pathology and neuroinflammatory processes in AD. Furthermore, the emergence of novel neuroinflammatory biomarkers offers promising avenues for earlier diagnosis and more effective monitoring of disease progression. Consequently, a substantial amount of ongoing research and numerous clinical trials are now focused on directly targeting neuroinflammation as a therapeutic strategy for AD. Despite the considerable progress in understanding the role of neuroinflammation, translating these insights into effective treatments presents several challenges, and future research will be crucial in overcoming these hurdles to develop meaningful therapies.

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