“…Modern pharmacological studies have showed that HLJDD could significantly modulate effects on age-related changes of the gene expressions in the hippocampus and cerebral cortex in SAMP8 model, which include genes that involved in different biological function and process: signal transduction (Dusp12, Rps6ka1, Rab26, Penk1, Nope, Leng8, Syde1, Phb, Def8, Ihpk1, Tac2, Pik3c2a), protein metabolism (Ttc3, Amfr, Prr6, Ube2d2), cell growth and development (Ngrn, Anln, Dip3b, Acrbp), nucleic acid metabolism (Fhit, Itm2c, Cstf2t, Ddx3x, Ercc5, Pcgfr6), energy metabolism (Stub1, Uqcr, Nsf ), immune response (C1qb), regulation of transcription (D1ertd161e, Gcn5l2, Ssu72), transporter (Slc17a7, mt-Co1), nervous system development (Trim3), and neurogila cell differentiation (Tspan2) [132]. In APPswe/PS1dE9 mice, another classic animal model of AD, HLJDD had positive effects on AD by ameliorating neuroinflammation and sphingolipid metabolic disorder [34]. In addition, HLJDD may inhibit the activity of indoleamine 2,3-dioxygenase, one of the potential participants involved in the pathogenesis of AD [133].…”