Traumatic brain injury and methamphetamine: A double-hit neurological insult

Hayek, Samer El; Allouch, Farah; Razafsha, Mahdi; Talih, Farid; Gold, Mark S.; Wang, Kevin; Kobeissy, Firas

doi:10.1016/j.jns.2020.116711

Cited by 15 publications

(6 citation statements)

References 187 publications

(257 reference statements)

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“…Taking METH in high doses can result in euphoria, delusions, hypersexuality, hyperthermia, cardiac arrhythmias, heart attacks, and kidney failure ( Glasner-Edwards and Mooney, 2014 ; Baradhi et al, 2019 ). The effects of long-term use of the drug can be permanent insomnia, brain damage, heart failure, and schizophrenia ( Dean et al, 2013 ; Thanos et al, 2016 ; El Hayek et al, 2020 ). In addition to being violent, METH addicts are prone to violent attacks, sexual assaults, robbery, and other crimes ( Sekine et al, 2006 ).…”

Section: Introductionmentioning

confidence: 99%

Molecular mechanisms of programmed cell death in methamphetamine-induced neuronal damage

et al. 2022

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Methamphetamine, commonly referred to as METH, is a highly addictive psychostimulant and one of the most commonly misused drugs on the planet. Using METH continuously can increase your risk for drug addiction, along with other health complications like attention deficit disorder, memory loss, and cognitive decline. Neurotoxicity caused by METH is thought to play a significant role in the onset of these neurological complications. The molecular mechanisms responsible for METH-caused neuronal damage are discussed in this review. According to our analysis, METH is closely associated with programmed cell death (PCD) in the process that causes neuronal impairment, such as apoptosis, autophagy, necroptosis, pyroptosis, and ferroptosis. In reviewing this article, some insights are gained into how METH addiction is accompanied by cell death and may help to identify potential therapeutic targets for the neurological impairment caused by METH abuse.

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Section: Introductionmentioning

confidence: 99%

Molecular mechanisms of programmed cell death in methamphetamine-induced neuronal damage

et al. 2022

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“…Previously, our research have focused on methamphetamine and MDMA drug of abuse where we indicated that these drugs would induce a similar phenotype as observed in traumatic brain injury (TBI) where we have demonstrated that METH and MDMA treatment would lead to neuronal protein structural injury as shown in several studies on TBI [35,58,[62][63][64]. Furthermore, applying psychoproteomics analysis on rat brain with methamphetamine highlighted the perturbed pathways involved in neuronal injury, neuroinflammation and altered cellular homeostasis which has been observed in deep proteomics studies applied on animals with TBI [24,[61][62][63][64][65][66][67].…”

Section: Discussionmentioning

confidence: 87%

“…[28,29,31,32]Moreover, the role of neuronal calcium signaling in mitochondrial dysfunction and the induction of neurotoxic cascades for SCs shown by Leong et al extends the link to SCs disrupting neuronal Ca2+ homeostasis leading to downstream mitochondrial dysfunction in dopaminergic neuronal SH-SY5Y cells. [33] Such studies have contributed to the understanding of the cathinone-induced neuronal damage but the evidence about forms of toxicity, apoptosis versus necrosis and the consequent involvement of neuroinflammatory processes of different SC drugs as compared to similar structure drugs like methamphetamine is scarce where these drugs such as methamphetamine has shown adverse effects on neural cells similar to what is observed in brain injury [9,34,35]. Hence, the paucity of scientific research and understanding of neurotoxic mechanisms determined the two-fold aims of the study where we: first, examine the effects of various doses of MDPV, butylone, and pyrovalerone on primary cultured neurons and astroglial cells by analyzing the mechanism of cell death using a cellular marker, neuroinflammatory effects and cellular oxidative stress; and second, assess SCs' behavioral and neuromodulatory effects by administering intraperitoneal (i.p.)…”

Section: Figure 1 Structures Of Cathinone Used In This Studymentioning

confidence: 99%

Effects of Cathinones (Bath Salts) On Cultured Primary Neurons/Astroglia Cells and Neurobehavioral Functions in Mice

Selig¹,

Pierre²,

Arja³

et al. 2022

Preprint

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This study aims to examine the cytotoxicity mechanisms of synthetic cathinone (bath salts) on rat primary cultured neurons and primary astroglial cells, and to assess their neurobehavioral effects on mice. We administered methylenedioxypyrovalerone (MDPV) to both rat primary cultured neurons and primary astroglial cells to assess cell injury. We also analyzed the effects of MDPV on these cell cultures using immunocytochemistry. We utilized western blotting to assess the breakdown of αII-spectrin and glial fibrillary acidic protein (GFAP) induced by MDPV. The western blotting experiment also included calpain and caspase inhibitors (SNJ1945 and Z-D-DCB, respectively) and pro-apoptotic and pro-necrotic agents (Staurosporine and calcium ionophore A23187, respectively). Lastly, we assessed MDPV’s effects on behavioral effects using rotarod, locomotor activity, elevated plus maze, Morris water maze, forced swimming, and open field tests. MDPV caused a dose-dependent release of LDH in both cerebrocortical neuron-astroglia mixed cultures and primary astroglial cultures. MDPV also caused neurite breakages and astroglial process retraction on immunocytochemistry. Lastly, MDPV induced αII-spectrin breakdown in western blotting experiments. Co-administration of calpain and caspase inhibitors reduced the degradation of αII-spectrin and GFAP. MDPV administration also increased anxiety-like behavior and locomotor activity in the mice. Synthetic cathinones, which share structural similarities with methamphetamine, also induce significant neurotoxic effects and neurobehavioral effects on rodent models. These neurotoxic effects are likely mediated by calpain and caspase-induced apoptosis and necrosis, while astroglial death is likely only due to calpain activation. Therefore, further research may focus on pharmacological interventions targeting these pathways to mitigate the cytotoxic impact of cathinones in humans.

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“…Previous studies have reported that low-dose METH pretreatment has a protective effect. For example, studies have found that the early use of low-dose METH pre-treatment could lower the neurological injury score of patients with craniocerebral injury (Duong et al, 2018;El Hayek et al, 2020). Low-dose METH pretreatment improved the cognitive functions of Alzheimer's patients (Shukla et al, 2019;Shukla and Vincent, 2020) and reduced the neurotoxic effects of high dose of METH (Lu et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-181a Is Involved in Methamphetamine Addiction Through the ERAD Pathway

Wang

Wei

Zhao

et al. 2021

Front. Mol. Neurosci.

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The regulation of microRNA (miRNA) is closely related to methamphetamine (METH) addiction. Past studies have reported that miR-181a is associated with METH addiction, but the mechanism pathways remain elusive. On the basis of our past studies, which reported the endoplasmic reticulum-associated protein degradation (ERAD) mediated ubiquitin protein degradation of GABAAα1, which was involved in METH addiction. The present study, using qRT-PCR and bioinformatics analysis, further revealed that miR-181a may be indirectly responsible for the METH addiction and downregulation of GABAAα1 through the regulation of ERAD.

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Traumatic brain injury and methamphetamine: A double-hit neurological insult

Cited by 15 publications

References 187 publications

Molecular mechanisms of programmed cell death in methamphetamine-induced neuronal damage

Molecular mechanisms of programmed cell death in methamphetamine-induced neuronal damage

Effects of Cathinones (Bath Salts) On Cultured Primary Neurons/Astroglia Cells and Neurobehavioral Functions in Mice

MicroRNA-181a Is Involved in Methamphetamine Addiction Through the ERAD Pathway

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