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The review also provides a useful tool to improve efficacy and functionality of fatty acid profiles in cosmetic applications.Patients with diabetes mellitus (DM) are more prone to develop cognitive decline and neurodegenerative diseases. A pathological association between an autosomal dominant neurological disorder caused by brain accumulation in mutated huntingtin (mHTT), known as Huntington disease (HD), and DM, has been reported. By using a diabetic mouse model, we previously suggested a central role of the metabolic pathways of HTT, further suggesting the relevance of this protein in the pathology of DM. Furthermore, it has also been reported that intranasal insulin (Ins) administration improved cognitive function in patients with neurodegenerative disorders such as Alzheimer disease, and that exendin-4 (Ex-4) enhanced lifespan and ameliorated glucose homeostasis in a mouse model of HD. Although antioxidant properties have been proposed, the underlying molecular mechanisms are still missing. Therefore, the aim of the present study was to investigate the intracellular pathways leading to neuroprotective effect of Ins and Ex-4 hypoglycemic drugs by using an in vitro model of HD, developed by differentiated dopaminergic neurons treated with the pro-oxidant neurotoxic compound 6-hydroxydopamine (6-ohda). Our results showed that 6-ohda increased mHTT expression and reduced HTT phosphorylation at Ser421, a post-translational modification, which protects against mHTT accumulation. Pre-treatment with Ins or Ex-4 reverted the harmful effect induced by 6-ohda by activating AKT1 and SGK1 kinases, and by reducing the phosphatase PP2B. AKT1 and SGK1 are crucial nodes on the Ins activation pathway and powerful antioxidants, while PP2B dephosphorylates HTT contributing to mHTT neurotoxic effect. In conclusion, present results highlight that Ins and Ex-4 may counteract the neurotoxic effect induced by mHTT, opening novel pharmacological therapeutic strategies against neurodegenerative disorders, with the main focus on HD, still considered an orphan illness.Introduction Pain is considered an unpleasant sensory and emotional experience, being considered as one of the most important causes of human suffering. Computational chemistry associated with bioinformatics has stood out in the process of developing new drugs, through natural products, to manage this condition. Objective To analyze, through literature data, recent molecular coupling studies on the antinociceptive activity of essential oils and monoterpenes. Data source Systematic search of the literature considering the years of publications between 2005 and December 2019, in the electronic databases PubMed and Science Direct. Eligibility criteria Were considered as criteria of 1) Biological activity non-clinical effects of an OE and/or monoterpenes on antinociceptive activity based on animal models and in silico analysis, 2) studies with plant material chemically characterized essential oils and/or their constituents isolated, 3) clinical and non-clinical studies with in silico analysis to assess antinocicerenergic, opioid, and serotonergic receptors, muscarinic receptors and GABAA opioid and serotonin receptors, 5-HT3 and M2 receptors. Many of the covered studies used molecular coupling to investigate the mechanism of action of various compounds, as well as molecular dynamics to investigate the stability of protein-ligand complexes. Conclusions The studies revealed that through the advancement of more robust computational techniques that complement the experimental studies, they may allow some notes on the identification of a new candidate molecule for therapeutic use.[This corrects the article DOI 10.3389/fphar.2020.00512.].Background Triple-negative breast cancer is a common malignant tumor with unfavorable prognosis affecting women worldwide; thus, there is an urgent need for novel therapeutic drugs with improved anti-tumor activity. Rac family small GTPase 1 (Rac1) plays an important role in malignant behavior and is a promising therapeutic target. We reported an anthraquinone compound, Rhein, and its derivative, 4F, and investigated their downregulation effects on Rac1 in breast cancer cells in vitro. [https://www.selleckchem.com/products/PP242.html Torkinib mTOR inhibitor] Methods The inhibition of cell proliferation by derivative 4F was investigated in two breast cancer (MDA-MB-231 and MCF-7) and normal breast (MCF-10A) cell lines by cell counting kit-8 assay and growth curves. The role of 4F in cell migration and invasion and cytoskeletal change were assessed by Transwell chamber assay and F-actin staining, respectively. The affinity of Rhein and its derivative for Rac1 protein and the regulation of Rac1 promoter activity were evaluated by molecular docking software and luciferase reporter gene assay, respectively. Rac1 protein expression was determined by western blot assay. Results Compared to Rhein, derivative 4F more strongly inhibited breast cancer cell proliferation, migration, and invasion and also cause cytoskeletal changes like those in paclitaxel. Derivative 4F not only bound more stably to Rac1 but also inhibited Rac1 promoter activity in cells and downregulated Rac1 protein expression. Conclusions Rhein derivative 4F is a new anthraquinone compound with better anti-tumor activity than that of the lead compound Rhein in breast cancer. It down-regulated Rac1 expression and may be a small molecule inhibitor of Rac1.Recent transcranial magnetic stimulation (TMS) research indicated that the ability of the dorsolateral prefrontal cortex (DLPFC) to disinhibit the contralateral primary motor cortex (M1) during motor preparation is an important predictor for bimanual motor performance in both young and older healthy adults. However, this DLPFC-M1 disinhibition is reduced in older adults. Here, we transiently suppressed left DLPFC using repetitive TMS (rTMS) during a cyclical bimanual task and investigated the effect of left DLPFC suppression (1) on the projection from left DLPFC to the contralateral M1; and (2) on motor performance in 21 young (mean age ± SD = 21.57 ± 1.83) and 20 older (mean age ± SD = 69.05 ± 4.48) healthy adults. As predicted, without rTMS, older adults showed compromised DLPFC-M1 disinhibition as compared to younger adults and less preparatory DLPFC-M1 disinhibition was related to less accurate performance, irrespective of age. Notably, rTMS-induced DLPFC suppression restored DLPFC-M1 disinhibition in older adults and improved performance accuracy right after the local suppression in both age groups.