Longitudinal characterization of biomechanical alterations in a Parkinson's disease mouse model using three-dimensional ground reaction forces.

OBJECTIVE

To longitudinally characterize locomotor biomechanical changes following unilateral intrastriatal α-Syn PFF inoculation in a Parkinson's disease mouse model and explore candidate the ground reaction force (GRF) based measures for their quantitative assessment.

METHODS

Based on biomechanical principles, this study analyzed the GRF of mice following α-Synuclein preformed fibril (PFF) inoculation to investigate longitudinal biomechanical indicators of changes in motor function after inoculation. A unilateral intrastriatal PFF injection mouse model was established, and a three-dimensional force sensor array was developed to measure GRF in control and PFF-injected mice at 0, 1, 3, and 6 months post-modeling. Independent-samples t-tests, one-way analysis of variance (ANOVA), and linear regression analysis were used to evaluate GRF and gait parameters.

RESULTS

At 0-months post-modeling, no significant differences in GRF or gait parameters were observed between the control and PFF groups. At 1-month post-inoculation, a significant difference in the maximum force-vector angle of the left hindlimb was observed, together with a separate difference in right forelimb GRF. At 3-months post-modeling, the PFF group exhibited prolonged gait-cycle and stance-phase durations, accompanied by reduced left-side GRF and pronounced bilateral asymmetry. At 6-months post-modeling, interlimb asymmetry further increased, particularly in the hindlimbs, whereas some between-group differences in gait parameters became less pronounced.

CONCLUSION

Three-dimensional GRF analysis revealed time-dependent changes in locomotor biomechanics following unilateral intrastriatal PFF inoculation. Parameters including GRF magnitude, force-vector angles, gait-cycle duration, stance-phase duration, and inter-limb asymmetry serve as candidate biomechanical markers for longitudinally characterizing motor dysfunction in mouse models of Parkinson's disease, though further validation in larger animal cohorts is required.