In addition, several studies described that D-galactoseinduced the accumulation of brain mitochondrial DNA mutation (Chen et al., 2011; Du et al., 2012; Du et al., 2015; Zeng et al., 2014) through: 1) decreasing DNA-repairing enzymes (OGG1, pol ᵧ) (Chen et al., 2011), and 2) common deletion of mitochondrial DNA and impairing mitochondrial structures via the NOX-dependent pathway (Du et al., 2015).
Effect of D-galactose-inducedapoptosis in the brain. D-galactose promoted the apoptotic process (Qian et al., 2008). In addition to apoptosis, D-galactosepromoted neuro-inflammation and neurodegeneration (Cui et al., 2006). The dosage from which D-galactose started inducing apoptosis was 100 mg- 500 mg/kg/day, duration was from 6 weeks to 9 weeks. (as shown in Table 2)
Effect of D-galactose-inducedbraininflammation. D-galactose started inducing inflammation at a dosage of 50mg-180mg/kg/day and duration was from 6 weeks to 60 days.
Therapeutic approaches to brain mitochondrial aginginduced by D-galactose:
The other therapeutic approaches to improvecognition with a dose-independent manner in the D-galactose model were fibroblast growth factor 21 (FGF21), salidroside, and tetrahydropalmatine (Banji et al., 2014; Gao et al., 2015; Kumar et al., 2009; Prakash and Kumar, 2013; Qu et al., 2016; Yang et al., 2016; Yu et al., 2015).