Altered neural cell junctions and ion-channels leading to disrupted neuron communication in Parkinson’s disease

Abstract

Parkinson’s disease (PD) is a neurological disorder that affects the movement of the human body. It is primarily characterized by reduced dopamine levels in the brain. The causative agent of PD is still unclear but it is generally accepted that α-synuclein has a central role to play. It is also known that gap-junctions and associated connexins are complicated structures that play critical roles in nervous system signaling and associated misfunctioning. Thus, our current article emphasizes how, alongside α-synuclein, ion-channels, gap-junctions, and related connexins, all play vital roles in influencing multiple metabolic activities of the brain during PD. It also highlights that ion-channel and gap-junction disruptions, which are primarily mediated by their structural-functional changes and alterations, have a role in PD. Furthermore, we discussed available drugs and advanced therapeutic interventions that target Parkinson’s pathogenesis. In conclusion, it warrants creating better treatments for PD patients. Although, dopaminergic replenishment therapy is useful in treating neurological problems, such therapies are, however, unable to control the degeneration that underpins the disease, thereby declining their overall efficacy. This creates an additional challenge and an untapped scope for neurologists to adopt treatments for PD by targeting the ion-channels and gap-junctions, which is well-reviewed in the present article.

Identification of a circRNA-miRNA-mRNA interactome associated with Parkinson’s Disease progression

“…Disruption in neuronal communication triggered by dysregulation in ion channel activity and cell junctions has previously been associated with the pathogenesis of PD [61]. Based on our analysis, we created an interactome network of the dysregulated circRNAs in samples from Parkinson's participants with their target miRNAs and downstream dysregulated gene targets.…”

Neurotransmitters in Type 2 Diabetes and the Control of Systemic and Central Energy Balance

“…GJs also regulate neural activity oscillations (i.e., maintaining a synchronized excitatory and inhibitory electrical activity) that allow robust communication between neuronal assemblies. Alterations in connexin GJ activities can impact their expression and function leading to the progression of neurodegenerative diseases, including AD and Parkinson’s disease and epilepsy [ 75 , 76 , 77 , 78 ].…”

Employing nanoparticle tracking analysis of salivary neuronal exosomes for early detection of neurodegenerative diseases

“…Generally, familial forms that are sporadic in origin but rare, are linked to mutations in SNCA, parkin, DJ-1, PINK-1 (PTEN-induced kinase 1), and Leucine-rich repeat kinase 2 (LRRK2) [10]. Although the detailed molecular pathogenesis is still unclear, it is widely accepted that α-syn plays a central role in causing PD pathology and is in turn responsible for neurodegeneration [11][12][13].…”