Abstract
Methamphetamine (METH), an illegal psycho-stimulant, is widely known as a recreational drug. In addition to its addictive effect, METH induces neurotoxicity via multiple mechanisms. The major contributors to METH-induced neurotoxicity are reactive oxygen species, which lead to cell death through apoptotic pathway and disturbances in mitochondria, the generation of neuroinflammation, and autophagy. Melatonin, a neurohormone secreted by the pineal gland, is a potent antioxidant compound that plays a beneficial role by protecting against the oxidative stress caused by METH. Melatonin also plays a role in maintaining mitochondrial homeostasis. Nanomolar concentrations of melatonin have been shown to protect against the inflammation caused by METH and to prevent the decrease in neurogenesis caused by METH in progenitor cells obtained from adult rat hippocampal tissue. The intent of this review is to describe the underlying mechanisms involving melatonin that protect against the neurodegeneration caused by METH.
Keywords: Melatonin, methamphetamine, neuroinflammation, autophagy, neurodegeneration, neurogenesis, neuroinflammation, oxidative stress, apoptosis.
Current Pharmaceutical Design
Title:Melatonin Attenuates Methamphetamine-Induced Neurotoxicity
Volume: 22 Issue: 8
Author(s): Pawaris Wongprayoon and Piyarat Govitrapong
Affiliation:
Keywords: Melatonin, methamphetamine, neuroinflammation, autophagy, neurodegeneration, neurogenesis, neuroinflammation, oxidative stress, apoptosis.
Abstract: Methamphetamine (METH), an illegal psycho-stimulant, is widely known as a recreational drug. In addition to its addictive effect, METH induces neurotoxicity via multiple mechanisms. The major contributors to METH-induced neurotoxicity are reactive oxygen species, which lead to cell death through apoptotic pathway and disturbances in mitochondria, the generation of neuroinflammation, and autophagy. Melatonin, a neurohormone secreted by the pineal gland, is a potent antioxidant compound that plays a beneficial role by protecting against the oxidative stress caused by METH. Melatonin also plays a role in maintaining mitochondrial homeostasis. Nanomolar concentrations of melatonin have been shown to protect against the inflammation caused by METH and to prevent the decrease in neurogenesis caused by METH in progenitor cells obtained from adult rat hippocampal tissue. The intent of this review is to describe the underlying mechanisms involving melatonin that protect against the neurodegeneration caused by METH.
Export Options
About this article
Cite this article as:
Wongprayoon Pawaris and Govitrapong Piyarat, Melatonin Attenuates Methamphetamine-Induced Neurotoxicity, Current Pharmaceutical Design 2016; 22 (8) . https://dx.doi.org/10.2174/1381612822666151214125657
DOI https://dx.doi.org/10.2174/1381612822666151214125657 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
Related Articles
-
Magnetic Field-Assisted Gene Delivery: Achievements and Therapeutic Potential
Current Gene Therapy Review of and Perspectives on the Toxicology of Graphene-based Materials
Current Drug Metabolism Reprogrammed Metabolism of Cancer Cells as a Potential Therapeutic Target
Current Pharmaceutical Design Oxidative Stress and NAD+ in Ischemic Brain Injury: Current Advances and Future Perspectives
Current Medicinal Chemistry Apoptosis Induction by Ultrasound and Microbubble Mediated Drug Delivery and Gene Therapy
Current Molecular Medicine The Past, Current Studies and Future of Organometallic <sup>99m</sup>Tc(CO)3 Labeled Peptides and Proteins
Current Pharmaceutical Design Gene Therapy Based on Lipid Nanoparticles as Non-viral Vectors for Glioma Treatment
Current Gene Therapy The Critical Role of Vascular Endothelial Growth Factor in Tumor Angiogenesis
Current Cancer Drug Targets Non Polymeric Nanoparticles for Photodynamic Therapy Applications: Recent Developments
Current Medicinal Chemistry Cancer Nanotechnology: Emerging Role of Gold Nanoconjugates
Anti-Cancer Agents in Medicinal Chemistry CXCR3-binding Chemokines: Novel Multifunctional Therapeutic Targets
Current Drug Targets - Immune, Endocrine & Metabolic Disorders Antiproliferative Efficacy of Angiotensin II Receptor Blockers in Prostate Cancer
Current Cancer Drug Targets Dysfunctions of the Diffusional Membrane Pathways Mediated Hemichannels in Inherited and Acquired Human Diseases
Current Vascular Pharmacology Paclitaxel Formulations: Challenges and Novel Delivery Options
Current Drug Delivery Use of the Bradykinin Agonist, Cereport as a Pharmacological Means of Increasing Drug Delivery to the CNS
Current Medicinal Chemistry - Immunology, Endocrine & Metabolic Agents Astrocytes as a 5-HT2B-Mediated SERT-Independent SSRI Target, Slowly Altering Depression-Associated Genes and Function
Current Signal Transduction Therapy Inhibition of Polo-Like Kinase 1 by BI2536 Reverses the Multidrug Resistance of Human Hepatoma Cells In Vitro and In Vivo
Anti-Cancer Agents in Medicinal Chemistry Hydrophobic Modification of Copper Nanospheres for Incorporation into Poloxamer Micelles, Aggregated Micellar Nanocages and Supramolecular Assemblies
Current Nanomedicine Utilising Nanotechnology and Nanosystems for Treatment of Rare Diseases
Pharmaceutical Nanotechnology Network Pharmacology and Reverse Molecular Docking-Based Prediction of the Molecular Targets and Pathways for Avicularin Against Cancer
Combinatorial Chemistry & High Throughput Screening