Literature DB >> 14714898

New therapeutics for the treatment of glycosphingolipid lysosomal storage diseases.

T D Butters1, R A Dwek, F M Platt.   

Abstract

Glycosphingolipid lysosomal storage diseases are a small but challenging group of human disorders to treat. Although these appear to be monogenic disorders where the catalytic activity of enzymes in glycosphingolipid catabolism is impaired, the presentation and severity of disease is heterogeneous. Treatment is often restricted to palliative care, but in some disorders enzyme replacement does offer a significant clinical improvement of disease severity. An alternative therapeutic approach termed "substrate deprivation" or "substrate reduction therapy" (SRT) aims to reduce cellular glycosphingolipid biosynthesis to match the impairment in catalytic activity seen in lysosomal storage disorders. N-Alkylated imino sugars are nitrogen containing polyhydroxylated heterocycles that have inhibitory activity against the first enzyme in the pathway for glucosylating sphingolipid in eukaryotic cells, ceramide-specific glucosyltransferase. The use of N-alkylated imino sugars to establish SRT as an alternative therapeutic strategy is described in cell culture and gene knockout mouse disease models. One imino sugar, N-butyl-DNJ (NB-DNJ) has been used in clinical trials for type 1 Gaucher disease and has shown to be an effective and safe therapy for this disorder. The results of these trials and the prospects of improvement to the design of imino sugar compounds for treating Gaucher and other glycosphingolipid lysosomal storage disorders will be discussed.

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Year:  2003        PMID: 14714898     DOI: 10.1007/978-1-4615-0065-0_14

Source DB:  PubMed          Journal:  Adv Exp Med Biol        ISSN: 0065-2598            Impact factor:   2.622


  5 in total

1.  Strategies for delivery of therapeutics into the central nervous system for treatment of lysosomal storage disorders.

Authors:  Silvia Muro
Journal:  Drug Deliv Transl Res       Date:  2012-06-01       Impact factor: 4.617

2.  Preimplantation diagnosis of a lysosomal storage disorder by in situ enzymatic activity: 'proof of principle' in acid sphingomyelinase-deficient mice.

Authors:  A Butler; S C Henderson; R E Gordon; A Dagan; S Gatt; E H Schuchman
Journal:  J Inherit Metab Dis       Date:  2005       Impact factor: 4.982

3.  Alpha versus beta: are we on the way to resolve the mystery as to which is the endogenous ligand for natural killer T cells?

Authors:  Y Ilan
Journal:  Clin Exp Immunol       Date:  2009-09-30       Impact factor: 4.330

4.  Modest phenotypic improvements in ASA-deficient mice with only one UDP-galactose:ceramide-galactosyltransferase gene.

Authors:  S Franken; D Wittke; J E Mansson; R D'Hooge; P P De Deyn; R Lüllmann-Rauch; U Matzner; V Gieselmann
Journal:  Lipids Health Dis       Date:  2006-08-07       Impact factor: 3.876

5.  Lysosomal Re-acidification Prevents Lysosphingolipid-Induced Lysosomal Impairment and Cellular Toxicity.

Authors:  Christopher J Folts; Nicole Scott-Hewitt; Christoph Pröschel; Margot Mayer-Pröschel; Mark Noble
Journal:  PLoS Biol       Date:  2016-12-15       Impact factor: 8.029

  5 in total

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