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Chronic exposure to these drugs depletes presynaptic monoamine stores, impairs long-term neuronal signaling, and induces neurodegeneration ( 4.2 Oxidative stress and mitochondrial dysfunction The excessive release of monoamines promotes ROS formation through the auto-oxidation of dopamine and norepinephrine

Preclinical studies further suggest that these cell-based autologous strategies may mitigate oxidative injury indirectly through paracrine regulation of redox-sensitive pathways and enhancement of the local reparative microenvironment (Imam et al., 2017

Active substance dependence: published trials in opioid- and alcohol-withdrawal contexts were small and used clinical settings, not self-directed protocols