Role of monoamine oxidase-B in Parkinson’s disease: implications for neurodegeneration and therapy

What is it about?

This review paper provides a comprehensive overview of the role of monoamine oxidase-B (MAO-B) in the pathogenesis of Parkinson’s disease (PD), focusing on its involvement in dopamine metabolism, oxidative stress, and neurodegeneration. It explores the biochemical mechanisms by which MAO-B contributes to neuronal damage, particularly through the generation of reactive oxygen species during dopamine catabolism. The paper also discusses the therapeutic relevance of MAO-B inhibitors, such as selegiline and rasagiline, which have shown neuroprotective and symptom-relieving effects in PD management. By integrating molecular, clinical, and pharmacological perspectives, the review highlights the significance of MAO-B as both a pathological factor and a therapeutic target in PD, offering insights for improved treatment strategies and future drug development.

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Photo by National Institute of Allergy and Infectious Diseases on Unsplash

Photo by National Institute of Allergy and Infectious Diseases on Unsplash

Why is it important?

This paper is important because it sheds light on the dual role of monoamine oxidase-B (MAO-B) in the progression of Parkinson’s disease, both as a contributor to dopaminergic neurodegeneration and as a target for therapeutic intervention. By elucidating how MAO-B-mediated oxidative stress accelerates neuronal loss, the review enhances understanding of PD pathophysiology. It also emphasizes the clinical relevance of MAO-B inhibitors, which are among the few available neuroprotective options in current treatment regimens. The paper bridges molecular mechanisms with therapeutic outcomes, guiding future research and drug development aimed at slowing disease progression and improving patient quality of life.

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