Increased ileal bile acid binding protein and galectin-9 are associated with mild cognitive impairment and Alzheimer's disease

Enterocyte damage and subsequent microbial translocation drive neuroinflammation in the pathogenesis of Alzheimer's disease (AD). Human ileal bile acid binding protein (I-BABP) and intestinal fatty acid binding proteins (I-FABP) are the indicators of enterocyte damage. Lipopolysaccharide-binding protein (LBP) is an indirect marker of microbial translocation. The activation of peripheral innate immune cells plays a crucial role in modulating AD progression. Galectin-9 is a versatile immunomodulatory molecule. The purpose of this study was to determine I-FABP, I-BABP, LBP, and galectin-9 levels in MCI and AD and investigate the relationship between I-FABP, I-BABP, LBP and galectin-9. In this study, I-FABP, I-BABP, LBP, and galectin-9 levels were measured using ELISA assay in 115 AD patients, 115 MCI patients, and 115 non-demented control subjects. Increased I-BABP and galectin-9 were observed in MCI and AD patients. Furthermore, AD patients had higher I-BABP and galectin-9 levels compared with MCI patients. However, I-FABP and LBP in three groups had no difference. I-BABP levels were positively correlated with galectin-9, after adjusting confounding factors (r = 0.409, p 0.001). In addition, multivariate analysis revealed that increased I-BABP and galectin-9 levels were significantly associated with reduced mini-mental state examination (MMSE) score. In conclusion, galectin-9 is correlated with I-BABP after adjusting confounding covariates. Moreover, increased I-BABP and galectin-9 in MCI and AD are significant factors for reduced MMSE score. Further studies are needed.