TY - JOUR
T1 - Current understanding of methamphetamine-associated dopaminergic neurodegeneration and psychotoxic behaviors
AU - Shin, Eun Joo
AU - Dang, Duy Khanh
AU - Tran, The Vinh
AU - Tran, Hai Quyen
AU - Jeong, Ji Hoon
AU - Nah, Seung Yeol
AU - Jang, Choon Gon
AU - Yamada, Kiyofumi
AU - Nabeshima, Toshitaka
AU - Kim, Hyoung Chun
N1 - Publisher Copyright:
© 2017, The Pharmaceutical Society of Korea.
PY - 2017/4/1
Y1 - 2017/4/1
N2 - Clinical and preclinical studies have indicated that chronic methamphetamine (MA) use is associated with extensive neurodegeneration, psychosis, and cognitive impairment. Evidence from animal models has suggested a considerable role of excess dopamine or glutamate, oxidative stress, neuroinflammation, and apoptosis in MA-induced neurotoxicity, and that protein kinase Cδ might mediate the interaction among these factors. In addition, the relatively long-lasting and recurrent nature of MA psychosis has been reproduced in animals treated with various dosing regimens of MA, which have shown behavioral sensitization, sociability deficits, and impaired prepulse inhibition. Genetic predisposition as well as dopaminergic and glutamatergic alterations might be important in the development of MA psychosis. Neuroimaging studies have identified functional and morphological changes related to the cognitive dysfunction shown in chronic MA users. Failure in the task-evoked phosphorylation of extracellular signal-related kinase likely underlies MA-induced memory impairment. Recent progress has suggested certain roles of oxidative stress and neuroinflammation in the psychosis and cognitive deficits induced by repeated low doses of MA. This review provides a comprehensive description of pertinent findings from human and animal studies, with an emphasis on the current understanding of the underlying mechanisms of MA neuropsychotoxicity and its relevance to Parkinson’s disease or schizophrenia.
AB - Clinical and preclinical studies have indicated that chronic methamphetamine (MA) use is associated with extensive neurodegeneration, psychosis, and cognitive impairment. Evidence from animal models has suggested a considerable role of excess dopamine or glutamate, oxidative stress, neuroinflammation, and apoptosis in MA-induced neurotoxicity, and that protein kinase Cδ might mediate the interaction among these factors. In addition, the relatively long-lasting and recurrent nature of MA psychosis has been reproduced in animals treated with various dosing regimens of MA, which have shown behavioral sensitization, sociability deficits, and impaired prepulse inhibition. Genetic predisposition as well as dopaminergic and glutamatergic alterations might be important in the development of MA psychosis. Neuroimaging studies have identified functional and morphological changes related to the cognitive dysfunction shown in chronic MA users. Failure in the task-evoked phosphorylation of extracellular signal-related kinase likely underlies MA-induced memory impairment. Recent progress has suggested certain roles of oxidative stress and neuroinflammation in the psychosis and cognitive deficits induced by repeated low doses of MA. This review provides a comprehensive description of pertinent findings from human and animal studies, with an emphasis on the current understanding of the underlying mechanisms of MA neuropsychotoxicity and its relevance to Parkinson’s disease or schizophrenia.
KW - Cognitive impairment
KW - Methamphetamine
KW - Neurotoxicity
KW - Psychosis
KW - Underlying mechanism
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U2 - 10.1007/s12272-017-0897-y
DO - 10.1007/s12272-017-0897-y
M3 - Review article
C2 - 28243833
AN - SCOPUS:85014015071
SN - 0253-6269
VL - 40
SP - 403
EP - 428
JO - Archives of Pharmacal Research
JF - Archives of Pharmacal Research
IS - 4
ER -