ABSTRACT
Emerging research extends the traditional understanding of monoamine oxidase-B (MAO-B)
beyond its role in dopamine metabolism, highlighting its significant contribution to
neuroinflammation and modulation of the glutamate system. This abstract explores the
multifaceted implications of MAO-B activity in neurodegenerative diseases and related
neurological disorders. Elevated MAO-B expression in reactive astrocytes, a hallmark of
neuroinflammation, results in increased production of reactive oxygen species (ROS) and the
exacerbation of inflammatory cascades. Concurrently, MAO-B influences glutamate
neurotransmission, impacting both glial glutamate uptake and neuronal glutamate release.
Consequently, aberrant MAO-B activity can contribute to excitotoxicity and disrupt synaptic
plasticity, further contributing to neuronal dysfunction. Understanding the intricate interplay
between MAO-B, neuroinflammation, and glutamate signaling provides a compelling rationale for
targeting MAO-B in therapeutic strategies aimed at mitigating neurodegenerative processes and
promoting neuronal health. This review discusses current evidence supporting the crucial role of
MAO-B in these interconnected pathways and explores potential avenues for targeted
interventions.
Keywords: MAO-B, Neuroinflammation, Glutamate, Dopamine.
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