Research Progress on the Pathogenesis of Parkinson's Disease and the Neuroregulatory Mechanism of Deep Brain Stimulation Based on Animal Models

Abstract

The core pathological features of Parkinson's disease (PD) are the loss of dopaminergic neurons in the compact part of the substantia nigra and the abnormal aggregation of α-synuclein; animal models can reproduce the pathological phenotype of this disease at multiple levels and serve as important tools for exploring its aetiology and evaluating intervention strategies. Deep brain stimulation (DBS) is currently widely used in the clinical management of motor symptoms in moderate-to-advanced Parkinson's disease; however, its complete regulatory mechanisms remain to be thoroughly elucidated. Based on relevant studies in animal models, this review summarizes a series of pathological changes, including dopaminergic neuron degeneration, abnormal α-synuclein aggregation, mitochondrial dysfunction, oxidative stress, neuroinflammation, and basal ganglia circuit dysregulation.This paper systematically reviews the experimental evidence supporting the regulatory role of deep brain stimulation (DBS) at multiple levels, including the correction of abnormal neural discharges, the attenuation of pathological neural oscillations, the modulation of neurotransmitter transmission, the remodelling of synaptic plasticity, and the intervention in neuroinflammation. Furthermore, the paper compares the differences between current animal models and the clinical features of Parkinson's disease in humans, and looks ahead to future directions such as closed-loop deep brain stimulation and precision neuromodulation