Biomolecules & Therapeutics
Methamphetamine-Induced Neuronal Damage: Neurotoxicity and Neuroinflammation
Buyun Kim, Jangmi Yun and Byoungduck Park*
College of Pharmacy, Keimyung University, Daegu 42601, Republic of Korea
Tel: +82-53-580-6653, Fax: +82-53-580-6645
Received: March 24, 2020; Revised: June 23, 2020; Accepted: June 25, 2020; Published online: July 15, 2020.
© The Korean Society of Applied Pharmacology. All rights reserved.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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.
Keywords: Methamphetamine, Neurotoxicity, Neuroinflammation, Excitotoxicity, Apoptosis

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