1. The WT group did not exhibit rightward rotation following APO administration.
2. In PD rats, there was an increase in walking time, along with a decrease in average speed and stride length.
3. However, these impairments were reversed after 20 days of L-DOPA administration.
4. Compared to WT, PD rats showed reduced grip strength, which was mitigated after 25 days of L-DOPA treatment.
5. Additionally, PD rats displayed decreased latency compared to WT, with L-DOPA administration reversing this reduction after 30 days.

Figure 4. Immunofluorescence (IF) analysis of tyrosine hydroxylase expression three weeks post-6-OHDA injection. Tyrosine hydroxylase (TH) is a crucial marker of dopaminergic neurons, and the reduction in TH expression is a hallmark of the disease's progression. The 6-OHDA was injected into the left side of the brain. As a result, no TH fluorescence (red fluorescence) was detected in the left substantia nigra and striatum, while the right substantia nigra and striatum still exhibited TH fluorescence. These findings confirm the successful establishment of the PD rat model.

Figure 6. The stride width and stride length of hMeCP2T158M mice at 11 to 12-week-old. Both male and female hMeCP2T158M mice displayed increased hindlimb stride width and decreased stride length, indicating impaired locomotion and coordination.

Figure 7. Tau expression in the hippocampal region was assessed across different mouse strains. Human tau, detected using the HT7 antibody, was observed in hMAPT WT, hMAPT P301L, and hMAPT P301S mice, but was absent in C57BL/6J mice. Consistently, hyperphosphorylated tau (AT8) was detected only in hMAPT P301L and hMAPT P301S mice, but not in hMAPT WT or C57BL/6J mice—indicating that tauopathy is associated with the P301L and P301S mutations. Neuronal nuclei were labeled with NeuN, and all nuclei were counterstained with DAPI. All mice were approximately 9 months old at the time of tissue collection.