Methamphetamine-Induced Neuronal Damage: Neurotoxicity and Neuroinflammation

被引:63
|
作者
Kim, Buyun [1 ]
Yun, Jangmi [1 ]
Park, Byoungduck [1 ]
机构
[1] Keimyung Univ, Coll Pharm, Daegu 42601, South Korea
基金
新加坡国家研究基金会;
关键词
Methamphetamine; Neurotoxicity; Neuroinflammation; Excitotoxicity; Apoptosis; VESICULAR MONOAMINE TRANSPORTER-2; ELEMENT-BINDING PROTEIN; ENDOPLASMIC-RETICULUM; DOPAMINE TRANSPORTER; SIGNALING PATHWAY; MICROGLIAL ACTIVATION; NUCLEUS-ACCUMBENS; SIGMA-1; RECEPTORS; OXIDATIVE STRESS; GENE-EXPRESSION;
D O I
10.4062/biomolther.2020.044
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Methamphetamine (METH) is a highly addictive psychostimulant and one of the most widely abused drugs worldwide. The continuous use of METH eventually leads to drug addiction and causes serious health complications, including attention deficit, memory loss and cognitive decline. These neurological complications are strongly associated with METH-induced neurotoxicity and neuroinflammation, which leads to neuronal cell death. The current review investigates the molecular mechanisms underlying METH-mediated neuronal damages. Our analysis demonstrates that the process of neuronal impairment by METH is closely related to oxidative stress, transcription factor activation, DNA damage, excitatory toxicity and various apoptosis pathways. Thus, we reach the conclusion here that METH-induced neuronal damages are attributed to the neurotoxic and neuroinflammatory effect of the drug. This review provides an insight into the mechanisms of METH addiction and contributes to the discovery of therapeutic targets on neurological impairment by METH abuse.
引用
收藏
页码:381 / 388
页数:8
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