Fig 2: Subgroup analyses of the relationship between air pollutants and CSF sTREM2. Scatter plots represent the associations of air pollutants and CSF sTREM2. CSF sTREM2 level was normalized and z scaled, and all air pollutants were z scaled. Linear models with adjustment of age, gender, educational level, and APOE‐ε4 carrier status were performed to detect potential modifying factors on the associations between air pollutants and CSF sTREM2. APOE, apolipoprotein E; CSF, cerebrospinal fluid; NO2, nitrogen dioxide; O3, ozone; PM2.5, fine particulate matter with diameter <2.5 μm; sTREM2, soluble TREM2.

Fig 3: CSF sTREM2 mediated associations between ambient PM2.5 and amyloid pathology. Mediation effects of CSF sTREM2 on AD pathology were estimated via 10,000 bootstrapped resamples with the adjustment of age, gender, educational level, and APOE‐ε4 status. The relationship between ambient PM2.5 and amyloid pathology (indicated by CSF Aβ42 [A] and CSF p‐tau/Aβ42 [B]) was mediated by CSF sTREM2. APOE, apolipoprotein E; Aβ42, amyloid beta‐peptide 42; CSF, cerebrospinal fluid; PM2.5, fine particulate matter with diameter <2.5 μm; p‐tau/Aβ42, the ratio of phosphorylated tau/amyloid beta‐peptide 42; sTREM2, soluble TREM2.

Fig 4: Representative images of tissue microarrays showing (A) strong and (B) low TREM2 expression in primary tumors of oral squamous cell carcinoma patients. Zoom images of selected regions from the cores are shown underneath.

Fig 5: The CSF and serums TREM-2 levels can be a specific MOG-AD diagnosis biomarker. (A,B) Receiver operating characteristic (ROC) curve analysis of sTREM2 in CSF and serum for MOG-AD diagnosis (N = 38). (A) The area under the curve (AUC) of CSF sTREM2 levels was 0.861 (p < 0.001). (B) The area under the curve (AUC) of serum sTREM2 levels was 0.812 (p = 0.001).