Chronic inflammation is a feature of Alzheimer´s disease (AD), resulting in excessive production of inflammatory mediators that can lead to neuroinflammation, contributing to alterations in Aβ production and deposition as Senile Plaques (SPs), and to neurofibrillary tangles (NFTs) formation, due to hyperphosphorylated Tau protein.

This work addressed the impact of the interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1), two chemokines, on Tau phosphorylation; and also evaluated the chemokines’ levels in plasma using samples from a regional cohort.

Human neuronal SH-SY5Y cells exposed to IL-8 and MCP-1 chemokines were monitored for their protein and phosphorylated protein levels by western blotting analysis. A serine/threonine protein phosphatase (PPs) activity assay was employed to monitor PPs activity. Subsequently, flow cytometry was used to monitor chemokines levels in plasma samples from individuals with cognitive deficits.

Chemokines’ exposure resulted only in minor cytotoxicity eg chronic inflammation can exacerbate this event. The work contributes to a better understanding of the mode of action of these chemokines on AD pathogenesis and opens novel research avenues.Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by the progressive loss of neurons leading to cognitive and memory decay. The main signs of AD include the irregular extracellular accumulation of amyloid-beta (Aβ) protein in the brain and the hyper-phosphorylation of tau protein inside neurons. Changes in Aβ expression or aggregation are considered key factors in the pathophysiology of sporadic and early-onset AD and correlate with the cognitive decline seen in patients with AD. Despite decades of research, current approaches in the treatment of AD are only symptomatic in nature and are not effective in slowing or reversing the course of the disease. COTI-2 in vivo Encouragingly, recent evidence revealed that exposure to electromagnetic fields (EMF) can delay the development of AD and improve memory. This review paper discusses findings from in vitro and in vivo studies that investigate the link between EMF and AD at the cellular and behavioural level, and highlights the potential benefits of EMF as an innovative approach for the treatment of AD.

Copy number variations (CNVs) play an important role in the genetic etiology of various neurological disorders, including Alzheimer’s disease (AD). Type 2 diabetes mellitus (T2DM) and major depressive disorder (MDD) were shown to have share mechanisms and signaling pathways with AD.

We aimed to assess CNVs regions that may harbor genes contributing to AD, T2DM, and MDD in 67 Saudi familial and sporadic AD patients, with no alterations in the known genes of AD and genotyped previously for APOE.

DNA was analyzed using the CytoScan-HD array. Two layers of filtering criteria were applied. All the identified CNVs were checked in the Database of Genomic Variants (DGV).

A total of 1086 CNVs (565 gains and 521 losses) were identified in our study. We found 73 CNVs harboring genes that may be associated with AD, T2DM or MDD. Nineteen CNVs were novel. Most importantly, 42 CNVs were unique in our studied cohort existing only in one patient. Two large gains on chromosomes 1 and 13 harbored genes implicated in the studied disorders. We identified CNVs in genes that encode proteins involved in the metabolism of amyloid-β peptide (AGRN, APBA2, CR1, CR2, IGF2R, KIAA0125, MBP, RER1, RTN4R, VDR and WISPI) or Tau proteins (CACNAIC, CELF2, DUSP22, HTRA1 and SLC2A14).

The present work provided information on the presence of CNVs related to AD, T2DM, and MDD in Saudi Alzheimer’s patients.

The present work provided information on the presence of CNVs related to AD, T2DM, and MDD in Saudi Alzheimer’s patients.Tumor cells frequently reprogram cellular metabolism from oxidative phosphorylation to glycolysis. Isocitrate dehydrogenase 2 (IDH2) has been intensely studied due to its involvement in the metabolic activity of cancer cells. Mutations in IDH2 promote neomorphic activity through the generation of oncometabolite 2-hydroxyglutarate (2-HG). The overproduced 2-HG can competitively inhibit α-KG-dependent dioxygenases to trigger cell differentiation disorders, a major cause of blood tumors. This review outlines recent progress in the identification of IDH2 inhibitors in blood cancer to provide reference for ongoing and future clinical studies.

To study the effects of blood glucose regulating compounds on human and rat sulfotransferases (SULTs) expressions.

Phase-II enzymes, sulfotransferases catalyze the sulfuryl-group-transfer to endogenous/exogenous compounds. The alteration of expressions of SULTs may have influence on the sulfation rate of their corresponding substrates.

The influence of the altered biotransformation property might impair or adjust several biochemical events, drug-drug interactions or modifications of bioaccumulation or excretion pattern of certain drug.

In this brief study, diabetes inducing drug streptozotocin (STZ 10 or 50 mg/kg to male Sprague Dawley rat for 2 weeks) or hyperglycemia controlling drug tolbutamide (TLB 0.1 or 10µM to human hepato-carcinoma cells, HepG2 for 10 days) was applied and the SULTs expressions were verified. Extensive protein-protein (STa, SULT2A1/DHEAST) interactions were studied by the STRING (Search-Tool-for-the-Retrieval-of-Interacting Genes/Proteins) Bioinformaticssoftware.

Present reslar glycemic regulation.

In brief, streptozotocin and tolbutamide, two glycaemia-modifying drugs demonstrate rat and human SULTs regulating activities. The reciprocal nature of these two drugs on SULTs expression may be associated with their contrasting abilities in glucose-homeostasis. Possible association of some SULT-isoform with hepatic fat-regulations may indicate an unfocused link between calorie-metabolism and the glycemic-state of the individuals. Explorations of this work may uncover the role of sulfation metabolism of any biomolecule on cellular glycemic regulation.

Recently, there has been increasing interest in nanomaterials processed using renewable and sustainable resources. Nanocellulose-based materials are of paramount value in the applications of biomedicine owing to their tailorable surface modification, favorable optical transparency, good hydrophilicity, excellent biocompatibility, and outstanding mechanical properties.

In the review, the recent advancements of nanocellulose, including cellulose nanofibers (CNFs), cellulose nanocrystals (CNCs), and bacterial cellulose (BC), are summarized, which are promising for biomedical applications.

By discussing different forms (one-dimensional (1D), two-dimensional (2D), and three-dimensional (3D)), the superiority of the nanocellulose-based materials with different constructed structures will be clarified for various biomedical applications, such as biosensing, drug delivery, wound dressing, and tissue engineering.

Furthermore, the challenges and prospects for future development of nanocellulose-based materials in biomedical applications are also discussed at the end in the review.