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Statins have transformed the treatment of cardiovascular diseases through primary and secondary prevention of events. Despite the success of statin's inefficient management of cardiovascular conditions, certain clinical trials, reviews, and meta-analysis point out that statins have the propensity to induce diabetes. The risk further increases with intensive statin therapy or in with patients with diabetes. A proper mechanism for the induction of the diabetic condition has not yet been determined. The involvement of statin with beta cells in insulin secretion and peripheral cells in insulin resistance has been widely studied and established. The present review provides an update on recent understanding of statin-induced diabetes. This covers the origin of statins, their development, possible mechanisms that explain the adverse effects in glucose homeostasis, and probable targets to remedy the condition. Glycogen synthase kinase 3 (GSK-3) is a serine/threonine kinase enzyme which controlled the neuronal functions such as neurite outgrowth, synapse formation, neurotransmission, and neurogenesis. The enzyme has two subunits as GSK-3α and GSK-3β. 4ACC, 1Q3D, 3AFG, 1UV5, 1Q5K are the important GSK-3 receptors isolated from Homo sapiens and Mus musculus. This enzyme mainly phosphorylates Tau protein with increased amount in neuronal fibres altogether with beta-amyloid plaques cause neuronal defects like Alzheimer, Parkinson's and many more. We investigated the developments of various synthetic GSK-3 inhibitors responsible for the prevention and treatment of neurological disorders like Alzheimer disease, bipolar disorders, antidepressant, neuroprotective etc. Results and Conclusion It was observed that structures of the GSK-3 inhibitors comprised of benzopyridine, benzthiazole, pyrazole, pyrazine, dioxolo-benzoxazin, oxadiazole, benzimidazole in the skeletal with cyclopropylamide, phenyl carbamothioate, 3-[(prohe effectivity of GSK-3, human adenosine kinase, cyclin dependent kinase, and phosphodiesterase-4 along with tail suspension test, forced swim test, percent neuronal survival and other cognitive behaviour. The observations confirmed the remarkable effects of the synthesized molecules to conquer Alzheimer, Parkinson's depression, psychosis and other forms of neurological disorders.The escalating emergence and prevalence of infections caused by multi-drug resistant (MDR) pathogenic bacteria accentuate the crucial need to develop novel and effectual therapeutic strategies to control this threat. Recent past surprisingly indicates a staggering decline in effective strategies against MDR. Different approaches have been employed to minimize the effect of resistance but the question still lingers over the astounding number of drugs already tried and tested to no avail, furthermore, the detection of new drug targets and the action of new antibacterial agents against already existing drug targets also complicate the condition. Antibiotic adjuvants are considered as one such promising approach for overcoming the bacterial resistance. Adjuvants can potentiate the action of generally adopted antibacterial drugs against MDR bacterial pathogens either by minimizing the impact and emergence of resistance or improving the action of antibacterial drugs. This review provides an overview of mechanism of antibiotic resistance, main types of adjuvants and their mode of action, achievements and progression.Flavonoids are chromene analogues abundantly found in plants. It is always of curiosity to discover natural flavonoid structures, since living things, including human, are routinely exposed to these compounds through many dietaries. Indeed, numerous studies conducted so far on flavonoids to display their diverse biological actions. The activity results obtained particularly on the effects of flavonoids on various validated and non-validated targets of Alzheimer's Disease (AD) make these compounds as promising agents either to be directly employed in clinical trials or to be utilized as important scaffolds for flavonoid based drug design studies. Although there are many review articles on the treatment and protective effects of flavonoids on AD, within this review, the effects of flavonoids on mitochondrial dysfunction developing throughout AD have been presented concomitant to their structural organization.In India as well as globally diabetes is in a state of high risk and only next to cardiovascular disease. As per the WHO the risk of diabetes is expected to rise to about 511 million by 2030. In quest for novel targets for type-2 diabetes many targets were elucidated such as Glycogen Synthase Kinase-3 (GSK-3), Dipeptidyl Peptidase (DPP-IV), PPAR-, α-Glucosidase, α-Amylase, GLP-1, SGLT. Among the targets GSK-3 reported to be an effective target for the treatment of diabetes. In the metabolism of glycogen, GSK is a regulating enzyme for the biosynthesis of glycogen (glycogenesis). It catalyzes the synthesis of linear unbranched molecule with 1,4-- glycosidic linkages. GSK-3 family has two isoenzymes, namely α and β which differ in their N- and C- terminal sequences and is a semi conservative multifunctional serine/threonine kinase enzyme. In this chapter we discuss an overview of general diabetic mechanisms and how GSK-3 modulation may influence these processes. Mutation in the GSK-3 complex that cause diabetes. Synthetic and natural scaffolds which modulates the GSK-3 against diabetes and lead optimization for the development of GSK-3 inhibitors. https://www.selleckchem.com/JAK.html This review mainly focuses on the development of GSK-3 inhibitors and highlights current and potential future therapeutic approaches that supports the notion of targeting glucose metabolism with novel antidiabetic agents.MicroRNAs (miRNAs) are non-coding RNAs containing around 22 nucleotides, which are expressed in vertebrates and plants. They act as posttranscriptional gene expression regulators, fine-tuning various biological processes in different cell types. There is emerging evidence on their role in different stages of atherosclerosis. In addition to regulating the inflammatory cells involved in atherosclerosis, miRNAs play fundamental roles in the pathophysiology of atherosclerosis such as endothelial cell (EC) dysfunction, the aberrant function of the vascular smooth muscle cell (VSMC) and cholesterol metabolism. Moreover, miRNAs participate in several pathogenic pathways of atherosclerotic plaque development, including their effects on immune cell signaling receptors and lipid uptake. In this study, we review our current knowledge of the regulatory role of miRNAs in various pathogenic pathways underlying atherosclerosis development and also outline potential clinical applications of miRNAs in atherosclerosis.

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