Abstract
BACKGROUND: Parkinson's disease (PD) is a progressive neurodegenerative disorder characterised by the degeneration of dopaminergic neurons in the substantia nigra pars compacta, resulting in motor symptoms such as tremor, rigidity and bradykinesia, along with cognitive impairments. While conventional research has largely focused on pathological degeneration, recent advances highlight the role of neuroplasticity-the brain's ability to reorganise and adapt neural circuits-as a potential mechanism for functional recovery and disease modification. SUMMARY: This review examines therapeutic strategies that enhance neuroplasticity in chronic Parkinson's disease mouse models. Key approaches discussed include neurotrophic factor (NTF) administration, deep brain stimulation (DBS), stem cell-based therapies and physical exercise. Evidence from experimental studies suggests that NTFs support dopaminergic neuron survival and synaptic repair, DBS modulates dysfunctional neural circuits and promotes adaptive plasticity, stem cell therapies offer both neuronal replacement and neurotrophic support, and physical exercise stimulates endogenous neuroplastic processes such as neurogenesis and synaptic reorganisation. Despite promising findings, variations in experimental design, disease severity and outcome measures across studies limit direct comparison and translation of results. KEY MESSAGE: Neuroplasticity-based interventions represent a promising avenue for slowing disease progression and improving functional outcomes in Parkinson's disease. Integrating pharmacological, neuromodulatory and behavioural approaches may enhance therapeutic efficacy, though further research is required to standardise protocols and facilitate clinical translation.