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Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the degeneration of dopaminergic neurons and motor dysfunction. The monoamine oxidase B (MAO-B) pathway plays a critical role in the pathogenesis of PD by contributing to neurodegeneration through oxidative stress. Precision medicine offers a transformative approach to PD treatment by leveraging genetic and molecular insights to tailor therapeutic strategies. This review explores the intersection of precision medicine and antipsychotic drugs in modulating the MAO-B pathway to mitigate PD symptoms. We discuss the biochemistry and function of MAO-B, its impact on disease progression, and the potential of genetic profiling to personalize treatment. Additionally, we examine the role of antipsychotic drugs, their mechanisms of action, and their interactions with the MAO-B pathway. The review highlights personalized approaches to MAO-B inhibition and the clinical evidence supporting these strategies. We address the challenges and limitations in implementing precision medicine, such as technical difficulties, drug interactions, and variability in patient responses. Finally, we explore future directions, including advances in precision medicine technologies and emerging therapies and their potential to enhance PD management. This review examines the indirect interaction between antipsychotics and the MAO-B pathway, highlighting how genetic variations and enzyme activity may influence drug efficacy, safety, and potential adverse effects, particularly when combined with MAO-B inhibitors in neuropsychiatric treatments.
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