![]() Eventually, activated PKB will phosphorylate and inhibit the action of GSK3β (glycogen synthase kinase 3β), a major kinase in the brain. Activation of PI3K and MAPK pathways result in the phosphorylation of protein kinase B (PKB) and extracellular signal-regulated kinases (ERKs), respectively. Similarly, the activated Gα proteins are also involved in the activation of the mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) pathways. In all mammals, cAMP has an important role in biological processes such as regulation of neurotransmitter synthesis, gene regulation, growth factors, immune function, hormone response, sensory input, and nerve transmission. When directed by the activated Gα-GTP complex, adenylyl cyclase acts as a catalyst for the synthesis of cAMP from ATP molecules, and phospholipase C acts as a catalyst for the synthesis of DAG and IP3 from the membrane lipid phosphatidyl inositol. The activated G-protein communicates a large number of second messenger small molecules, especially adenylyl and phospholipase C, to initiate and coordinate intracellular signaling pathways ( Figure 1). In its active form, both the complex and dimer structures relay messages within the cell by interacting with other membrane proteins (second messengers) such as cyclic adenosine monophosphate (cAMP), diacylglycerol (DAG), and inositol-1,4,5-triphosphate (IP3). This process replaces GDP with GTP in the Gα subunit, and eventually dissociates into Gα-GTP complex and Gβγ dimer, both attached to the plasma membrane. ![]() ![]() However, on binding with any extracellular signals (active stage), a conformational change is observed in GCPR that leads to G-protein activation. In the absence of signaling molecules (inactive stage), GDP attaches to the Gα-subunit, and the whole Gα-GDP complex is bound to a nearby GPCR. Gα-subunit binds either to guanosine triphosphate or guanosine diphosphate, depending on the nature of its activity. There are four main classes of G proteins: Gi that inhibits adenylyl cyclase Gs that activates adenylyl cyclase Gq that activates phospholipase C and G12 and G13, of unknown function. G-proteins are heterotrimeric with three subunits made up of α, β and γ subunits. This entry aims to provide researchers and devel-opers a comprehensive idea about the different receptors involved in AD pathogenesis that may lead to finding a new therapeutic strategy to treat AD. This re-view gives an overall idea centering on major receptors, their agonist and antagonist and future prospects of viral mimicry in AD pathology. In this regard, this entry summarizes the role of receptors as a potential target for treating AD and focuses on the path of major receptors which are responsible for AD progression. Current ap-proaches focus on symptomatic treatments to maintain AD patients’ mental stability and behav-ioral symptoms by decreasing neuronal degeneration however, the complexity of AD patholo-gy requires a wide range of therapeutic approaches for both preventive and curative treatments. Despite the identification of Aβ plaques and NFTs as biomarkers for Alzheimer’s disease (AD) pathology, therapeutic interventions remain elusive, with neither an absolute prophylactic nor a curative medication available to impede the progression of AD presently available.
0 Comments
Leave a Reply. |
Details
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |