![]() In addition to other mechanisms, α-synuclein also forms an amyloidogenic, helix structure that interacts with membrane lipids of the brain and this interaction can be exploited further for the treatment of PD. PD is pathologically characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) accompanied by Lewy bodies, i.e. There are seven known causative alleles for familial PD: α-synuclein (SNCA), glucocerebrosidase (GBA), leucine-rich repeat kinase 2 (LRRK2), vacuolar protein sorting-associated protein 35 (VPS35), parkin RBR E3 ubiquitin-protein ligase (PARK2), phosphatase, and tensing homolog-induced kinase 1 (PARK7) 4, 5. Genetic PD accounts for 10–15% of overall occurrences, while all others are categorized as sporadic 3. There are two main types of PD: hereditary, which is biologically acquired either in an autosomal dominant or recessive way, and sporadic (idiopathic), which is thought to emerge through genomic and environmental interactions 2. Parkinson’s disease (PD) is a progressing neurological ailment that causes mortality and impacts 1–3% of the worldwide community around the age of 60 years 1. 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. 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. In conclusion, it warrants creating better treatments for PD patients. ![]() Furthermore, we discussed available drugs and advanced therapeutic interventions that target Parkinson’s pathogenesis. 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. 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 is also known that gap-junctions and associated connexins are complicated structures that play critical roles in nervous system signaling and associated misfunctioning. The causative agent of PD is still unclear but it is generally accepted that α-synuclein has a central role to play. ![]() ![]() It is primarily characterized by reduced dopamine levels in the brain. Parkinson’s disease (PD) is a neurological disorder that affects the movement of the human body. ![]()
0 Comments
Leave a Reply. |
Details
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |