Moreover, lipid accumulation induced by APOE4 has been shown to disrupt microglial communication with neurons, further elucidating the mechanisms by which APOE4 contributes to AD pathology (ref: Victor doi.org/10.1016/j.stem.2022.07.005/). The phenomenon of mosaic loss of Chromosome Y in aged human microglia has been linked to age-related diseases, including AD, suggesting that chromosomal alterations may influence microglial function and disease progression (ref: Vermeulen doi.org/10.1101/gr.276409.121/). Additionally, therapeutic approaches targeting neuroinflammation, such as the use of molecular chaperones against β-amyloid toxicity, have shown promise in ameliorating AD pathology in mouse models, indicating potential avenues for intervention (ref: Manchanda doi.org/10.1016/j.ymthe.2022.08.010/). Overall, these findings underscore the complex interplay between microglial function, genetic factors, and therapeutic strategies in the context of Alzheimer's disease.

Furthermore, the anti-inflammatory cytokine interleukin-37 (IL-37) has been shown to reduce neuroinflammation and cognitive impairment in AD mouse models, suggesting that immunomodulatory therapies could provide a dual benefit by addressing both inflammation and cognitive decline (ref: Lonnemann doi.org/10.7554/eLife.75889/). The synthetic peroxisome proliferator-activated receptor (PPAR) agonist DTMB has also demonstrated efficacy in alleviating chronic microglial inflammation and reducing amyloid pathology, indicating that targeting metabolic pathways may offer additional therapeutic avenues (ref: Oh doi.org/10.1007/s13311-022-01275-y/). Lastly, the modulation of gut microbiota through probiotics has emerged as a novel strategy to alleviate cognitive impairments and amyloid accumulation in AD models, emphasizing the importance of the microbiota-gut-brain axis in neurodegenerative diseases (ref: Wang doi.org/10.1002/mnfr.202200265/). Collectively, these studies illustrate the diverse and innovative therapeutic strategies targeting microglial function in the context of Alzheimer's disease.

Moreover, the phenomenon of mosaic loss of Chromosome Y in aged microglia has been linked to increased susceptibility to neurodegenerative diseases, including AD, suggesting that chromosomal alterations may influence microglial function and immune responses (ref: Vermeulen doi.org/10.1101/gr.276409.121/). Innovative imaging techniques have revealed that microglia may not directly induce oxidative stress at amyloid plaques but instead form protective barriers, indicating a more nuanced role in the neuroinflammatory landscape of AD (ref: Wendt doi.org/10.1016/j.redox.2022.102448/). Additionally, the modulation of gut microbiota has been shown to influence neuroinflammation and cognitive function, further emphasizing the importance of systemic immune interactions in the pathophysiology of AD (ref: Zhang doi.org/10.3233/JAD-220532/). These findings collectively underscore the intricate relationship between neuroinflammation, immune responses, and the progression of Alzheimer's disease.

Furthermore, the phenomenon of mosaic loss of Chromosome Y in aged microglia has been linked to various age-related diseases, including AD, suggesting that chromosomal alterations may play a role in the aging process and its impact on neuroinflammation (ref: Vermeulen doi.org/10.1101/gr.276409.121/). The exploration of alternative splicing events in microglia has also revealed novel pathological mechanisms in AD, providing insights into how genetic variations may influence microglial responses and contribute to disease progression (ref: Lu doi.org/10.18632/aging.204223/). These findings collectively underscore the critical role of genetic and molecular factors in shaping microglial function and their implications for Alzheimer's disease.

Moreover, the use of probiotics, such as Lactobacillus plantarum MA2, has demonstrated potential in alleviating cognitive deficits and regulating gut microbiota in AD models, indicating that dietary interventions may offer therapeutic benefits (ref: Wang doi.org/10.1002/mnfr.202200265/). The interplay between gut microbiota, inflammation, and cognitive function underscores the importance of considering systemic factors in the management of AD. Additionally, the anti-inflammatory properties of natural compounds like andrographolide have been shown to attenuate neuroinflammation and cognitive impairment in AD models, further supporting the role of dietary components in influencing neurodegenerative outcomes (ref: Souza doi.org/10.1007/s12640-022-00569-5/). Collectively, these findings highlight the intricate connections between the microbiota-gut-brain axis and Alzheimer's disease, suggesting that targeting this axis may provide novel therapeutic strategies.

Additionally, the structural elucidation of polysaccharides from Polygala tenuifolia has revealed their anti-neuroinflammatory properties, suggesting that traditional herbal remedies may offer therapeutic benefits in managing cognitive decline associated with AD (ref: Zeng doi.org/10.1016/j.ijbiomac.2022.08.161/). The exploration of 1-L transcription in AD has also provided new insights into the molecular mechanisms by which β-amyloid peptides may influence neuronal and microglial interactions, further elucidating the complexity of neurodegenerative processes (ref: Nahalka doi.org/10.3390/cimb44080243/). These findings collectively underscore the multifaceted nature of neurodegenerative mechanisms and their impact on cognitive impairment in Alzheimer's disease.

Moreover, the engineering of anti-TREM2 antibodies has shown potential in promoting amyloid plaque clearance by enhancing microglial function, indicating a novel therapeutic strategy that could also serve as a biomarker for monitoring treatment efficacy (ref: Zhao doi.org/10.1080/19420862.2022.2107971/). Additionally, the modulation of gut microbiota through dietary interventions has been linked to improvements in cognitive function and neuroinflammation, suggesting that microbiota-derived metabolites may serve as biomarkers for AD progression and treatment response (ref: Zhang doi.org/10.3233/JAD-220532/). These advancements in biomarker discovery and diagnostic approaches highlight the potential for integrating neuroinflammatory markers and microbiota profiles in the early detection and management of Alzheimer's disease.