Current understanding of methamphetamine-associated dopaminergic neurodegeneration and psychotoxic behaviors

다국어 초록 (Multilingual Abstract)

Clinical and preclinical studies have indicatedthat chronic methamphetamine (MA) use is associated withextensive neurodegeneration, psychosis, and cognitiveimpairment. Evidence from animal models has suggested aconsiderable role of excess dopamine or glutamate,oxidative stress, neuroinflammation, and apoptosis in MAinducedneurotoxicity, and that protein kinase Cd mightmediate the interaction among these factors. In addition,the relatively long-lasting and recurrent nature of MApsychosis has been reproduced in animals treated withvarious dosing regimens of MA, which have shownbehavioral sensitization, sociability deficits, and impairedprepulse inhibition. Genetic predisposition as well asdopaminergic and glutamatergic alterations might beimportant in the development of MA psychosis. Neuroimagingstudies have identified functional andmorphological changes related to the cognitive dysfunctionshown in chronic MA users. Failure in the task-evokedphosphorylation of extracellular signal-related kinaselikely underlies MA-induced memory impairment. Recentprogress has suggested certain roles of oxidative stress andneuroinflammation in the psychosis and cognitive deficitsinduced by repeated low doses of MA. This review providesa comprehensive description of pertinent findingsfrom human and animal studies, with an emphasis on thecurrent understanding of the underlying mechanisms ofMA neuropsychotoxicity and its relevance to Parkinson’sdisease or schizophrenia.

참고문헌 (Reference)

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