| Abstract: | Objective:Fibrosis-related biomarkers, such as Fibroblast growth factor 23 (FGF-23) and Galectin-3, have been shown to promote myocardial fibrosis and arterial stiffness. However, it remains unknown whether these biomarkers contribute to the development of cognitive dysfunction.Design and method:A total of 822 seniors (aged >= 60 years) participated in the sixth wave survey of the Cardiovascular Disease Risk Factors Two-Township study and received the Mini-Mental State Examination (MMSE) to evaluate the global cognitive function. Carotid-femoral pulse wave velocity (cf-PWV) was measured using carotid and femoral arterial tonometry. Correlation coefficients (crude and partial) and Logistic regression were used to evaluate the association of cardiac FGF-23 and Galectin-3 for lower cognitive performance (MMSE less than 26).Results:FGF-23 and Galectin-3 were independently associated with MMSE after adjustment for age, sex, and education (Pearson r = −0.156 [p-value <0.0001] and −0.205 [p < 0.0001], respectively). The multivariable models with adjusted age, sex, education, brachial systolic blood pressure, glucose and low-density lipoprotein revealed the odds ratio (OR) of lower cognitive performance was 3.11 (95% confidence intervals: 1.52–6.40) for the 4th, 1.58 (0.76–3.28) for the 3rd, and 1.37 (0.64–2.93) for the 2nd quartile of Galectin-3, respectively, and 4.60 (2.19–9.65) for 4th, 1.59 (0.72–3.52) for 3rd, and 1.61 (0.72–3.62) for 2nd quartiles of FGF-2, compared to the reference groups (1st quartiles). Such associations remained after adjusting for eGFR and cf-PWV. Higher FGF-23 (OR = 2.99 [1.78–5.03] for 4th quartile vs. Others) and high Galectin-3 (OR = 2.00 [1.17–3.42] for 4th quartile vs. Others) were independently associated with lower cognitive performance. Those with higher FGF-23 plus higher GLA3 had 6.70 -fold risk (3.21–13.98) for lower cognitive function, compared to those with lower FGF-23 plus lower Galectin-3.Conclusions:Both FGF-23 and Galectin-3 were independently associated cognitive function, which suggested the role of ventricular-arterial fibrosis in the pathophysiology of dementia. |
