The amyloid/tau/neurodegeneration (ATN) biomarker framework has greatly progressed the diagnosis and staging of Alzheimer's disease (AD). However, recent research highlights neuroinflammation as an equally critical factor in AD pathology across humans, rodents, and non‐human primates (NHPs). This review evaluates the combined use of ATN and neuroinflammatory biomarkers—such as glial fibrillary acidic protein (GFAP) (astrocytic marker) and triggering receptor expressed on myeloid cells 2 (TREM2)/ ionized calcium‐binding adapter molecule 1 (IBA‐1) (microglial markers)—in elucidating AD mechanisms, promoting early diagnosis, and shaping therapeutic strategies. It also summarizes the key features and translational potential of NHP models that closely mimic human AD pathology, highlighting the promising prospects of integrating these models with the ATN(X) biomarker system. These insights strengthen the link between biomarkers, NHP research, and clinical practice, opening new avenues for the early detection and treatment strategies of AD.Highlights: Neuroinflammation biomarkers, including glial fibrillary acidic protein (GFAP), triggering receptor expressed on myeloid cells 2 (TREM2)/sTREM2, and YKL‐40, show strong clinical potential in Alzheimer's disease (AD). Incorporating neuroinflammation biomarkers into the ATN(X) framework may enhance diagnostic precision. Advanced non‐human primate (NHP) models closely replicate human brain pathology, addressing key limitations of mouse models. Measuring ATN(X) biomarkers in NHPs may improve clinical translation and support early diagnosis of AD. Optimizing NHP models—including ApoE4 status, injection protocols, and gene‐editing approaches—is crucial for reproducibility and efficiency.

Background: Poststroke depression (PSD) is the most frequent neuropsychiatric consequence of stroke. Electroacupuncture (EA) has been found to be an effective therapy for treating PSD. However, the underlying mechanisms of EA’s efficacy remain unclear. This research aimed to investigate the effects of EA on alterations in gut microbiota and fecal metabolome in PSD rats. Methods: Analyses of gut microbiome and fecal metabolome were performed to identify gut microbes and their functional metabolites in a sham group, PSD group, and EA group. We conducted enrichment analysis to identify the differential metabolic pathways in three groups. Correlations between altered gut microbes and differential metabolites after EA treatment were studied. Results: PSD showed decreased species-richness/diversity indices of microbial composition, characterized by an increase in Muribaculaceae, Peptostreptococcaceae, Oscillospiraceae, Ruminococcaceae, and Clostridiaceae and a decrease in Lactobacillaceae, Lachnospiraceae, and Bacteroidaceae. Of these, the abundance of Muribaculaceae, Lactobacillaceae, Lachnospiraceae, Peptostreptococcaceae, and Clostridiaceae were reversed by EA. Furthermore, PSD was associated with 34 differential fecal metabolites, mainly belonging to steroid hormone biosynthesis, that could be regulated by EA. Conclusion: Regulation of gut microbiome and lipid metabolism could be one of the potential mechanisms for EA treatment for alleviating the depressive behaviors of PSD.

Cognitive impairment poses a significant burden on individuals, families, and society worldwide. Despite the lack of effective treatment strategies, emerging evidence suggests that the microbiome–gut–brain (MGB) axis may play a critical role in the pathogenesis of cognitive impairment. While targeted treatment is not yet comprehensive, recently, acupuncture and moxibustion therapy has participated increasingly in the treatment of degenerative diseases and has achieved a certain therapeutic effect. In this review, the possible mechanisms by which acupuncture and moxibustion therapy may improve cognitive impairment through the MGB axis are reviewed, including regulating gut microbial homeostasis, improving intestinal inflammation mediated by the neuroendocrine–immune system, and enhancing intestinal barrier function. We also discuss common acupoints and corresponding mechanism analysis to provide insights into further exploration of mechanisms that target the MGB axis and thereby intervene in cognitive impairment.

Introduction: Extracorporeal circulation (ECC) is essential in cardiac surgery but triggers severe complications like systemic inflammation, coagulopathy, and end-organ damage. Progress in understanding these events has been hampered by the high cost and complexity of medium-animal models, alongside the technical challenges of operating on mice. Methods: To address this, we developed a miniaturized, pre-configured murine ECC system that reliably recapitulates key clinical sequelae of ECC. This novel model, established in C57BL/6 mice, utilizes a low-cost, single-use circuit to maximize reproducibility and minimize contamination. Throughout the procedure, key physiological parameters were monitored and maintained stable. Results: Our system successfully induced hallmark acute-phase responses to ECC, including a systemic inflammatory response (leukocytosis and elevated pro-inflammatory cytokines including IL-1β, IL-6, TNF-α, and IL-18), consumptive coagulopathy (thrombocytopenia), and metabolic stress (elevated lactate levels and electrolyte disturbances). Additionally, early biomarkers associated with organ stress were detected, including elevated cardiac troponin and LDH, increased serum creatinine, elevated AST, and increased pulmonary myeloperoxidase activity. Discussion: With stable core temperature and pH underscoring the system’s controllability, this model provides a reproducible experimental platform for investigating the early molecular mechanisms of ECC-induced systemic responses and for supporting preclinical evaluation of potential therapeutic interventions in cardiovascular research.