Advantages of Structure-Based Drug Design Approaches in Neurological Disorders

Abstract

Objective: The purpose of the review is to portray the theoretical concept on neurological disorders from research data.Background: The freak changes in chemical response of nerve impulse causes neurological disorders. The research evidence of the effort done in the older history suggests that the biological drug targets and their effective feature with responsive drugs could be valuable in promoting the future development of health statistics structure for improved treatment for curing the nervous disorders.Methods: In this review, we summarized the most iterative theoretical concept of structure based drug design approaches in various neurological disorders to unfathomable understanding of reported information for future drug design and development.Results: On the premise of reported information we analyzed the model of theoretical drug designing process for understanding the mechanism and pathology of the neurological diseases which covers the development of potentially effective inhibitors against the biological drug targets. Finally, it also suggests the management and implementation of the current treatment in improving the human health system behaviors.Conclusion: With the survey of reported information we concluded the development strategies of diagnosis and treatment against neurological diseases which leads to supportive progress in the drug discovery.

Multifaceted Roles of GSK‐3 in Cancer and Autophagy‐Related Diseases

“…When WNTs bind their frizzled receptors, through the key transducer Dishevelled (DVL) phosphoprotein, stabilization and accumulation of β -catenin occur; this event is dependent on GSK-3 inhibition due to phosphorylation at a residue different from that targeted by AKT [ 3 ]. In fact, although AKT signaling leads to inhibition of GSK-3 via serine phosphorylation, AKT signaling does not cause stabilization and accumulation of β -catenin [ 9 , 10 ]. It has also shown β -catenin accumulation in the presence of highly active GSK-3, and this is dependent on APC or β -catenin mutations [ 11 , 12 ].…”

Editorial: Improving Neuropharmacology using Big Data, Machine Learning and Computational Algorithms

“…Authors further discuss different neurological disease modalities including Alzheimer’s disease, Niemann-Pick type C disease, REM-RBD, ALS, epilepsy, dementia, migraine, and stroke. The review offers an excellent balance between the clinical, biochemical and bioinformatics methods and thus could help students, researchers and clinicians to understand various inter-disciplinary aspects of drug development [ 36 ].…”

Integrated Transcriptome Profiling Identifies Prognostic Hub Genes as Therapeutic Targets of Glioblastoma: Evidenced by Bioinformatics Analysis

“…As a result, additional surgery is required for definitive tissue diagnosis, or inappropriately waiting for radiographic findings to change as the disease progresses leads to more patient deaths. 12 , 13 Thus, there is a dire need for more sensitive and specific tumor biomarkers for the early detection of gliomas. On the other hand, literature surveys demonstrate that gene expression profiling affords an unbiased technique to classify tumors and its correlation is more satisfactory than tumor histology, with prognosis.…”

“…Unfortunately, the detection of anatomic changes in the face of progressing or regressing disease is often nonspecific and slow to change by these imaging modalities. As a result, additional surgery is required for definitive tissue diagnosis, or inappropriately waiting for radiographic findings to change as the disease progresses leads to more patient deaths. , Thus, there is a dire need for more sensitive and specific tumor biomarkers for the early detection of gliomas. On the other hand, literature surveys demonstrate that gene expression profiling affords an unbiased technique to classify tumors and its correlation is more satisfactory than tumor histology, with prognosis. , Various specific tumor-related biomarkers have been found to better understand the molecular pathogenesis of GBM due to the development of next-generation sequencing technology. , Some molecular signatures including IDH mutation (favorable prognoses, secondary GBM), copy number variations of chromosomes 9 and 10 and of the telomerase reverse transcriptase promoter gene (TERTp), B-Raf gene (BRAF) and H3F3A mutation, O6-methylguanine-DNA methyltransferase (MGMT) promoter methylation, and 1p/19q co-deletion (chemosensitivity)­11 have been clinically used for the detection of gliomas. , However, the molecular biomarkers were limited in specific classification and precise outcomes in the prediction of GBM. , Therefore, there is an urgent need to identify novel molecular biomarkers and new therapeutic strategies to improve the diagnostics and prognosis of GBM and elucidate the mechanisms of GBM or increase overall patient survival.…”