The effect of sodium channels on neurological/neuronal disorders: A systematic review

Abstract

Neurological and neuronal disorders are associated with structural, biochemical, or electrical abnormalities in the nervous system. Many neurological diseases have not yet been discovered. Interventions used for the treatment of these disorders include avoidance measures, lifestyle changes, physiotherapy, neurorehabilitation, pain management, medication, and surgery. In the sodium channelopathies, alterations in the structure, expression, and function of voltage-gated sodium channels (VGSCs) are considered as the causes of neurological and neuronal diseases. Online databases, including Scopus, Science Direct, Google Scholar, and PubMed were assessed for studies published between 1977 and 2020 using the keywords of review, sodium channels blocker, neurological diseases, and neuronal diseases. VGSCs consist of one α subunit and two β subunits. These subunits are known to regulate the gating kinetics, functional characteristics, and localization of the ion channel. These channels are involved in cell migration, cellular connections, neuronal pathfinding, and neurite outgrowth. Through the VGSC, the action potential is triggered and propagated in the neurons. Action potentials are physiological functions and passage of impermeable ions. The electrophysiological properties of these channels and their relationship with neurological and neuronal disorders have been identified. Subunit mutations are involved in the development of diseases, such as epilepsy, multiple sclerosis, autism, and Alzheimer's disease. Accordingly, we conducted a review of the link between VGSCs and neurological and neuronal diseases. Also, novel therapeutic targets were introduced for future drug discoveries.

Prospects of Intravenous CoenzymeQ10 Administration in Emergency Ischemic Conditions

“…Additionally, CoQ10 regulates the activity of NO synthases [4]. Studies have demonstrated that coenzyme Q10 exhibits both inhibitory effects on iNOS and eNOS, as evidenced by Erol B in 2009 [6], 2 and stimulatory effects, as confirmed in an experimental rat model of seizures with the activation of constitutive NOS [7].…”

“…It also regulates the activity of NFkB nuclear transcription factors, impacting the activity of inflammosomes and reducing the production of pro-inflammatory cytokines. CoQ10 is involved in apoptosis and mitophagy processes, in particular in regulation of the activity of apoptosis proteins [4,5].…”

“…Regarding the use of CoQ10 in various neurological diseases to assess its impact on neurologic symptoms, multilple reviews have been presented [2,4,19]. The analysis of Co Q10 efficacy in clinical neurology practice, in comparison to experimental results, highlights the necessity for higher doses and longer courses of CoQ10 therapy [4].…”

“…Regarding the use of CoQ10 in various neurological diseases to assess its impact on neurologic symptoms, multilple reviews have been presented [2,4,19]. The analysis of Co Q10 efficacy in clinical neurology practice, in comparison to experimental results, highlights the necessity for higher doses and longer courses of CoQ10 therapy [4]. In patients with acute cerebral blood flow disorders, oral administration of CoQ10 at a daily dose of 300 mg significantly improved MMSE scale and NIH Stroke Scale mental status scores [36].…”

Inhibition of NaV1.7: the possibility of ideal analgesics

“…Non-selective VGSC inhibitors have been studied for decades, and their utility has been proven in clinical settings. 42–44,50 Their common characteristics are weak VGSC inhibitory activity with modest subtype selectivity. Their inhibitory activity is usually in the micromolar range.…”