Abstract
Methamphetamine (METH), an amphetamine-type psychostimulant, is highly abused worldwide. Chronic abuse of METH causes neurodegenerative changes in central dopaminergic neurons with numerous neuropsychiatric consequences. Neuronal apoptosis plays a critical role in METH-induced neurotoxicity and may provide promising pharmacological targets for preventing and treating METH addiction. In recent years, accumulating evidence has revealed that natural products may possess significant potentials to inhibit METH-evoked neuronal apoptosis. In this review, we summarized and analyzed the improvement effect of natural products on METH-induced neuronal apoptosis and their potential molecular mechanisms on modulating dopamine release, oxidative stress, mitochondrial-dependent apoptotic pathway, endoplasmic reticulum stress-mediated apoptotic pathway, and neuroinflammation. Hopefully, this review may highlight the potential value of natural products in modulating METH-caused neuronal apoptosis and provide useful information for future research and developments of novel and efficacious pharmacotherapies in this field.
Highlights
Methamphetamine (METH), known as “ice” or “crystal,” is one of the most widely used and abused illicit amphetamine-type stimulants (Courtney and Ray, 2014; Jones et al, 2020)
Most of the METH-elicited neuropsychiatric consequences are attributable to its neurotoxicity, including direct damage to central dopaminergic and serotonergic terminals and the subsequent neurodegenerative changes upon the activation of neuronal autophagy, apoptosis, and necrosis (Davidson et al, 2001; Yu et al, 2015; Sanchez et al, 2018)
Important progress has been achieved in interpreting the complex mechanism underlying METH-produced neurotoxicity
Summary
Methamphetamine (METH), known as “ice” or “crystal,” is one of the most widely used and abused illicit amphetamine-type stimulants (Courtney and Ray, 2014; Jones et al, 2020). Natural products may garner considerable neuroprotective properties and effectively mitigate neurodegeneration of Parkinson’s disease that partially shares pathogenesis with METH-induced apoptosis, including dopamine release, oxidative stress, and mitochondria damage (Rios et al, 2016; Solayman et al, 2017). Their application may merit further research and development as a promising strategy for pharmacological intervention against METH-induced neuronal apoptosis. Multiple pathways are involved in the complicated mechanism of METH-caused neurotoxicity, and oxidative stress has been considered an essential contributor to neuronal apoptosis
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