Unraveling the Molecular Tapestry: Mechanisms Underlying Methamphetamine-Induced Neurodegeneration, Inflammation, and Neurotoxicity

Abstract

Methamphetamine (METH) abuse continues to pose a significant public health concern, with chronic use leading to severe neurological consequences. This abstract explores the intricate molecular mechanisms driving METH-induced neurodegeneration, inflammation, and neurotoxicity. By dissecting the complex interplay of neurotransmitter dysregulation, oxidative stress, and neuroinflammatory responses, we elucidate how METH disrupts neuronal integrity and function. Additionally, we delve into emerging research on the role of glial cells and immune mediators in exacerbating neuronal damage. Understanding these mechanisms is crucial for developing effective therapeutic strategies to mitigate METH-induced neurotoxicity and alleviate the burden of addiction-related neurological disorders. This review delves into the intricate molecular mechanisms that underlie METH-induced neurodegeneration, inflammation, and neurotoxicity. The multifaceted pathways, through which METH exerts its toxic effects on neuronal populations, including oxidative stress, mitochondrial dysfunction, excitotoxicity, and neuroinflammation, are explored. Additionally, the role of glial cells, particularly microglia and astrocytes, in perpetuating neuroinflammatory responses following METH exposure is discussed. A comprehensive understanding of the molecular landscape of METH neurotoxicity is critical for the development of effective interventions to combat the deleterious effects of METH abuse on brain health.