Morin Mitigates Methamphetamine-Induced Neurotoxicity: Effects on Motor and Cognitive Function.

INTRODUCTION

Neurodegenerative diseases are a major public health concern, often associated with motor and cognitive deficits. Methamphetamine (METH) exposure induces lasting neurological impairment and neuronal loss. This study evaluated Morin's potential to reverse these effects, focusing on motor and cognitive dysfunction in METH-induced neurotoxicity.

METHODS

Adult rats were randomly assigned into seven groups, including control, Morin-only, METH-only, METH plus fluoxetine, and three groups receiving METH followed by varying doses of Morin. Following METH induction, Morin, a natural flavonoid with antioxidant properties, was administered to rats. Neurobehavioral tests evaluated motor and cognitive function; serum levels of oxidative stress markers, inflammatory cytokines, dopamine, and acetylcholine were measured. Histological and immunohistochemical analyses of the basal ganglia were performed to evaluate neuronal integrity.

RESULTS

METH exposure significantly elevated oxidative stress and inflammatory markers, altered neurotransmitter levels, and impaired both motor and cognitive performance, coinciding with neuronal loss in the basal ganglia. Treatment with Morin ameliorated these effects in a dose-dependent manner. Neuronal degenerative features noted in the METH-only group were significantly ameliorated in the Morin-treated groups.

CONCLUSION

These findings indicate that Morin mitigates METH-induced neurotoxicity by reducing oxidative stress, and suppressing inflammation. This study demonstrates Morin's potential as a treatment option for the neurological effects of methamphetamine misuse.