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Natural Product Compounds from Plants in Neurodegenerative Diseases
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Priya Darshani, Md TanjimAlam, Prem P. Tripathi, V.S. Pragadheesh
Polyphenolic compounds such as phenolic acids, flavonoids, stilbenes, alkaloids, catechins, carotenoids, and terpenes have important roles in treating neurodegenerative diseases. Glycan-based therapies have found their way in treating ALS and other neurodegenerative disorders. Lesser amounts of fucosylated glycans and higher amounts of sialylated glycans have been reported in the serum of ALS patients. Furthermore, cerebrospinal fluid IgG N-glycosylation has been indicated as a potential biomarker for ALS. Also, a carbohydrate sulfotransferase, GlcNAc6ST1, is found to be overexpressed and belongs to one of the topmost 40 ALS relevant genes in microglia (Wang et al., 2019).
Macular Corneal Dystrophy: An Updated Review
Published in Current Eye Research, 2021
Shalini Singh, Sujata Das, Chitra Kannabiran, Saumya Jakati, Sunita Chaurasia
MCD appears to be the result of a metabolic abnormality in keratan sulfate.20 Keratan sulfate is found in the corneal epithelium, Bowman’s membrane, keratocytes, Descemet membrane and endothelium. Carbohydrate sulfotransferase (CHST6) gene on chromosome 16(16q22) gene is explained to be important in producing sulfated keratan sulfate which is important glycosoaminoglycan in the adult cornea. CHST6 gene encodes N-acetylglucosamine 6-0-sulfotransferase, an enzyme which transfers sulfate to the unsulfated keratin chains on lumican.21,22 Lumican preserves the crucial size, ordered structure, impacts corneal hydration and hence the corneal transparency. This explains the stromal haze and the loss of corneal transparency due to mutation in CHST6 gene in MCD.
Inflammatory bowel disease: new therapies from antisense oligonucleotides
Published in Annals of Medicine, 2018
Irene Marafini, Giovanni Monteleone
The pathogenesis of fibro-strictures, one of the major complications in CD [74], is not fully understood. However, fibrosis is supposed to be the late stage of an inflammation-driven process resulting in an altered balance between matrix deposition and degradation by specific enzymes [75]. Thus, enzymes controlling matrix remodelling could represent therapeutic targets in stricturing CD. Carbohydrate sulphotransferase 15 (CHST15) is a putative type II transmembrane Golgi enzyme, which catalyses sulphation of chondroitin sulphate (CS) to produce E-disaccharide units, which bind to various pro-inflammatory and pro-fibrotic mediators, adhesion molecules, receptors for advanced glycation end-product and pathogenic microorganisms [76]. Oversulfated CS enhances collagen deposition and binds to type V collagen, a subtype of collagen that accumulates in CD intestinal strictures [77]. CHST15 is increased in the colon of active CD patients [78]. Altogether, these observations support the potential involvement of CHST15 in intestinal fibrogenesis.
Bilateral phototherapeutic keratectomy for corneal macular dystrophy in an adolescent: case report and review of the literature
Published in Ophthalmic Genetics, 2020
Melissa Shields, Jamie E. Craig, Emmanuelle Souzeau, Aanchal Gupta
While the diagnosis of MCD was historically made by the typical clinical appearance of stromal deposits, advances in molecular genetics have identified causative variants in the carbohydrate sulfotransferase 6 gene (CHST6) (3). CHST6 encodes for the enzyme catalysing the sulfation of N-acetyl glucosamine residues which are critical for the formation keratan sulfate in corneal keratocytes. There is resulting irregular collagen fibrillar arrangement, accumulation of unsulfated keratin sulfate in keratocytes and corneal stroma, and progressive corneal opacification. Heterozygous variant carriers do not exhibit corneal pathology.