Mitochondrial Dysfunction in Chlorpromazine (Induced) Neurodegeneration

Abstract

Chlorpromazine CPZ, a widely used antipsychotic, has been linked to neurological side effects, including tardive dyskinesia, and evidence suggests a potential for long-term neurotoxic effects. This review synthesizes findings from in vitro and in vivo studies investigating the impact of CPZ exposure on mitochondrial bioenergetics, oxidative stress, mitochondrial dynamics, and mitophagy. Studies were identified through comprehensive searches of databases such as PubMed, Scopus, and Web of Science using relevant keywords. The available literature indicates that CPZ can disrupt mitochondrial function, leading to decreased ATP production, increased reactive oxygen species (ROS) generation, impairments in mitochondrial fusion and fission, and altered mitophagy. These disruptions contribute to neuronal damage and cell death. Further investigation is crucial to fully elucidate the mechanisms by which CPZ affects mitochondrial integrity and contributes to neurodegeneration. This review highlights the importance of mitochondrial dysfunction as a key pathological mechanism in CPZ-induced neurotoxicity. Understanding these pathways may provide valuable insight for developing strategies to mitigate the neurodegenerative potential of CPZ and related antipsychotic medications.