High Fibroblast Growth Factor 23, Sialic Acids, and Albumin Modulation in Alzheimer’s Patients

Abstract

Background: Alzheimer’s disease (AD) is a prevalent form of dementia, posing significant health and societal burdens. Pathologically characterized by neurofibrillary tangles and senile plaques, it lacks definitive diagnostic markers. Fibroblast growth factor (FGF)23 and Sialic Acids (Sias) are implicated in cell signaling and antioxidative defense, while lipid peroxidation (LPO) is linked to neurodegeneration. The aim of this study was to assess serum levels of Fibroblast Growth Factor 23 (FGF23), Malondialdehyde (MDA) as a marker of lipid peroxidation, Sialic Acids (Sias), and albumin in Alzheimer's disease (AD) patients compared to age-matched healthy controls. Method: A case-control study involving 17 AD patients and 17 healthy controls investigated serum levels of FGF23, Sias, malondialdehyde (MDA), and albumin. Biochemical assays and statistical analyses were conducted. Results: Biochemical analyses revealed a significant increase in serum FGF23 and MDA levels in AD patients compared to controls (p < 0.05). Additionally, AD patients exhibited lower levels of serum Sias and albumin. Furthermore, in the patient group, serum MDA levels were inversely correlated with normalized global gray matter volume (GMV), adjusted for age, sex, and Child-Pugh class. Conclusion: This study underscores the potential of FGF23, MDA, Sias, and albumin as biomarkers for AD. Further research elucidating their roles in AD pathogenesis is warranted. Decreased FGF23 in AD may involve disrupted phosphate regulation and neuroprotection mechanisms. Elevated MDA suggests increased lipid peroxidation, contributing to neuronal damage. Reduced Sias may impair antioxidative defense, exacerbating oxidative stress. Low albumin levels correlate with cognitive decline and oxidative damage in AD.