Similarly, reduced serum sialic acid levels were linked to impaired antioxidative defenses and higher oxidative damage, alongside altered levels of fibroblast growth factor 23 (FGF23) and albumin, supporting the notion that both hypo- and hypersialylation may reflect different stages or systemic responses in Alzheimer’s disease pathogenesis [59]. Here, FGF23 is linked to early-onset autosomal dominant Alzheimer disease.