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The blood-brain barrier (BBB) is considered an important protective barrier in the central nervous system (CNS). The barrier is mainly formed by endothelial cells (ECs) interconnected by various junctions such as tight junctions (TJs), gap junctions, and adherent junctions. They collectively constitute an intensive barrier to the transit of different substances into the brain, selectively permitting small molecules to pass through by passive movement but holding off large ones such as peptides and proteins to cross the brain. Hence some molecules selectively transfer across the BBB by active routes via transcytosis. The BBB also forms a barrier against neurotoxins as well as pathogenic agents. Although various CNS disorders like Alzheimer's disease (AD), and Parkinson's disease (PD) could hamper the integrity of the border. Nevertheless, the BBB acts as a barrier for CNS disorders treatment because it prevents the drugs from reaching their target in the CNS. In recent years, different strategies, including osmotic disruption of BBB or chemical modification of drugs, have been used to transfer the chemotherapeutic agents into brain substances. Nowadays, nanoparticles (NPs) have been used as an effective and non-invasive tool for drug delivery and diagnosis of CNS disorders. In this review, we discuss the structural characteristic of BBB, safe passageways to cross the BBB, and the relation of barrier lesions with different CNS disorders. In the end, we explore various progresses in drug delivery, diagnosis, imaging, and treatment of CNS disorders using nanoparticles.

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: Quantum dots (QDs) are nanoparticles (NPs) with electronic and optical properties such as emitting bright light and fluorescence. They also carry specific characters such as photostability, high quantum yield, high emission, and size-turnable. Nowadays, a great interest is given to the extensive use of theranostic-NPs for sensing and imaging, as well as drug delivery. Moreover, QDs may yield great potential for the diagnosis and treatment of various central nervous system (CNS) diseases (e.g., Parkinson’s disease, Alzheimer’s disease, and multiple sclerosis). The blood-brain barrier (BBB) protects the brain tissue. Only certain small molecules like water and gases can cross BBB, whereas larger molecules enter via receptors, but many drugs are incapable of passing the barrier. A series of great advances have been achieved concerning using different NPs (e.g., QDs) to deliver drugs to the brain and CNS imaging. In this review, we discussed a wide variety of QDs along with their production, passive or active delivery of therapeutic agents for neurodegenerative diseases, and different image production.

Background: Celiac disease (CeD) is an autoimmune enteropathy triggered by dietary gluten. Almost 90% of CeD patients have HLA-DQ2 or -DQ8 haplotypes. As a high proportion of first-degree relatives (FDRs) of CeD patients have the same haplotype, it is assumed that they are at a higher risk of disease development than the general population. Nevertheless, the prevalence of CeD among FDRs is considerably low (7.5%). Methods: In order to figure out this discrepancy, a microarray dataset of intestinal mucosal biopsies from CeD, FDR, and control groups was reanalyzed, and gene co-expression network using WGCNA was constructed. The differentially expressed genes in the opposite modules from the consensus analysis were applied for functional enrichment analysis. Results: WGCNA analysis identified 10 consensus modules in both CeD and FDR groups, including 5 modules with opposite correlation. Among the genes of opposing modules, 159 of them were identified as commonly differentially expressed genes with an adjusted p-value< 0.05 between FDR and CeD groups. Functional enrichment analysis revealed the significant contributions of these genes in host energy metabolism, programmed cell death, antigen cross presentation, and actin folding. In a deep view to the relation of actin folding to celiac disease occurrence, it was found that misfolding of actin and presentation of anti-actin antibodies occur in CeD patients. The current study reports that this pathway is oppositely regulated in FDR group and this might be a trigger for celiac manifestation. Conclusions: The consensus signaling pathways with opposing expression patterns identified in this study give us a clue about the gene circuits that are dysregulated in celiac patients. Considering the prominent relation of actin folding to disease occurrence and its opposite manner in celiac patients and healthy individuals, it is proposed that targeting CCT/TriC chaperonin family might result in a reduction of misfolded actin and the production of autoantibodies.