Targeting Neurobiological Mechanisms in Parkinson’s Disease: Implications for Current and Emerging Therapies.

This research examines Parkinson’s disease as a biologically complex and heterogeneous neurodegenerative disorder, emphasizing how variations in genetic, epigenetic, and cellular mechanisms shape disease onset, progression, and treatment response. By synthesizing existing literature on dopaminergic degeneration, alpha-synuclein aggregation, Lewy body pathology, and gut–brain axis involvement, the study highlights how Parkinson’s cannot be understood as a single uniform condition. Instead, it presents the disease as a spectrum of subtypes, including “brain-first” and “body-first” models, each with distinct pathological trajectories and clinical manifestations.

The paper adopts a comprehensive review-based approach, drawing on genetic studies, genome-wide association data, and neurobiological research to examine how heterogeneity influences symptom presentation and therapeutic outcomes. It discusses how current treatments primarily dopamine replacement strategies—provide symptomatic relief but fail to modify disease progression. The analysis also explores the limitations of existing therapeutic models and emphasizes the role of genetic variants, epigenetic influences, and environmental exposures in shaping individual disease profiles.

Overall, the study argues for a shift toward precision medicine in Parkinson’s care. By aligning emerging therapies with specific neurobiological mechanisms, genetic profiles, and disease subtypes, the research highlights opportunities for more effective, personalized interventions. The paper ultimately underscores the need to move beyond symptom management toward disease-modifying strategies that address the underlying biological complexity of Parkinson’s disease.