Literature DB >> 34652821

Sorbitol Is a Severity Biomarker for PMM2-CDG with Therapeutic Implications.

Anna N Ligezka1,2, Silvia Radenkovic1,3,4,5, Mayank Saraswat6,7,8, Kishore Garapati6,7,8,9, Wasantha Ranatunga1, Wirginia Krzysciak2, Hitoshi Yanaihara10, Graeme Preston1, William Brucker11, Renee M McGovern12, Joel M Reid12, David Cassiman3,13, Karthik Muthusamy1, Christin Johnsen1, Saadet Mercimek-Andrews14,15, Austin Larson16, Christina Lam17,18, Andrew C Edmondson19, Bart Ghesquière4,5, Peter Witters13,20, Kimiyo Raymond6, Devin Oglesbee6, Akhilesh Pandey6, Ethan O Perlstein21, Tamas Kozicz1,6, Eva Morava1,6,13.   

Abstract

OBJECTIVE: Epalrestat, an aldose reductase inhibitor increases phosphomannomutase (PMM) enzyme activity in a PMM2-congenital disorders of glycosylation (CDG) worm model. Epalrestat also decreases sorbitol level in diabetic neuropathy. We evaluated the genetic, biochemical, and clinical characteristics, including the Nijmegen Progression CDG Rating Scale (NPCRS), urine polyol levels and fibroblast glycoproteomics in patients with PMM2-CDG.
METHODS: We performed PMM enzyme measurements, multiplexed proteomics, and glycoproteomics in PMM2-deficient fibroblasts before and after epalrestat treatment. Safety and efficacy of 0.8 mg/kg/day oral epalrestat were studied in a child with PMM2-CDG for 12 months.
RESULTS: PMM enzyme activity increased post-epalrestat treatment. Compared with controls, 24% of glycopeptides had reduced abundance in PMM2-deficient fibroblasts, 46% of which improved upon treatment. Total protein N-glycosylation improved upon epalrestat treatment bringing overall glycosylation toward the control fibroblasts' glycosylation profile. Sorbitol levels were increased in the urine of 74% of patients with PMM2-CDG and correlated with the presence of peripheral neuropathy, and CDG severity rating scale. In the child with PMM2-CDG on epalrestat treatment, ataxia scores improved together with significant growth improvement. Urinary sorbitol levels nearly normalized in 3 months and blood transferrin glycosylation normalized in 6 months.
INTERPRETATION: Epalrestat improved PMM enzyme activity, N-glycosylation, and glycosylation biomarkers in vitro. Leveraging cellular glycoproteome assessment, we provided a systems-level view of treatment efficacy and discovered potential novel biosignatures of therapy response. Epalrestat was well-tolerated and led to significant clinical improvements in the first pediatric patient with PMM2-CDG treated with epalrestat. We also propose urinary sorbitol as a novel biomarker for disease severity and treatment response in future clinical trials in PMM2-CDG. ANN NEUROL 20219999:n/a-n/a.
© 2021 American Neurological Association.

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Year:  2021        PMID: 34652821      PMCID: PMC8820356          DOI: 10.1002/ana.26245

Source DB:  PubMed          Journal:  Ann Neurol        ISSN: 0364-5134            Impact factor:   10.422


  29 in total

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3.  Phosphomannomutase deficiency is a cause of carbohydrate-deficient glycoprotein syndrome type I.

Authors:  E Van Schaftingen; J Jaeken
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4.  Long-term clinical effects of epalrestat, an aldose reductase inhibitor, on progression of diabetic neuropathy and other microvascular complications: multivariate epidemiological analysis based on patient background factors and severity of diabetic neuropathy.

Authors:  N Hotta; R Kawamori; M Fukuda; Y Shigeta
Journal:  Diabet Med       Date:  2012-12       Impact factor: 4.359

5.  Biallelic mutations in SORD cause a common and potentially treatable hereditary neuropathy with implications for diabetes.

Authors:  Andrea Cortese; Yi Zhu; Adriana P Rebelo; Sara Negri; Steve Courel; Lisa Abreu; Chelsea J Bacon; Yunhong Bai; Dana M Bis-Brewer; Enrico Bugiardini; Elena Buglo; Matt C Danzi; Shawna M E Feely; Alkyoni Athanasiou-Fragkouli; Nourelhoda A Haridy; Rosario Isasi; Alaa Khan; Matilde Laurà; Stefania Magri; Menelaos Pipis; Chiara Pisciotta; Eric Powell; Alexander M Rossor; Paola Saveri; Janet E Sowden; Stefano Tozza; Jana Vandrovcova; Julia Dallman; Elena Grignani; Enrico Marchioni; Steven S Scherer; Beisha Tang; Zhiqiang Lin; Abdullah Al-Ajmi; Rebecca Schüle; Matthis Synofzik; Thierry Maisonobe; Tanya Stojkovic; Michaela Auer-Grumbach; Mohamed A Abdelhamed; Sherifa A Hamed; Ruxu Zhang; Fiore Manganelli; Lucio Santoro; Franco Taroni; Davide Pareyson; Henry Houlden; David N Herrmann; Mary M Reilly; Michael E Shy; R Grace Zhai; Stephan Zuchner
Journal:  Nat Genet       Date:  2020-05-04       Impact factor: 41.307

6.  Japanese Clinical Practice Guideline for Diabetes 2016.

Authors:  Masakazu Haneda; Mitsuhiko Noda; Hideki Origasa; Hiroshi Noto; Daisuke Yabe; Yukihiro Fujita; Atsushi Goto; Tatsuya Kondo; Eiichi Araki
Journal:  J Diabetes Investig       Date:  2018-03-26       Impact factor: 4.232

7.  High N-glycan multiplicity is critical for neuronal adhesion and sensitizes the developing cerebellum to N-glycosylation defect.

Authors:  Daniel Medina-Cano; Ekin Ucuncu; Lam Son Nguyen; Michael Nicouleau; Joanna Lipecka; Jean-Charles Bizot; Christian Thiel; François Foulquier; Nathalie Lefort; Catherine Faivre-Sarrailh; Laurence Colleaux; Ida Chiara Guerrera; Vincent Cantagrel
Journal:  Elife       Date:  2018-10-12       Impact factor: 8.140

Review 8.  Aldose Reductase Inhibitors of Plant Origin in the Prevention and Treatment of Alcoholic Liver Disease: A Minireview.

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9.  Repurposing the aldose reductase inhibitor and diabetic neuropathy drug epalrestat for the congenital disorder of glycosylation PMM2-CDG.

Authors:  Sangeetha Iyer; Feba S Sam; Nina DiPrimio; Graeme Preston; Jan Verheijen; Kausalya Murthy; Zachary Parton; Hillary Tsang; Jessica Lao; Eva Morava; Ethan O Perlstein
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  5 in total

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3.  Why rare disease needs precision medicine-and precision medicine needs rare disease.

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4.  Genotype-Phenotype Correlations in PMM2-CDG.

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Review 5.  Systematic Review: Drug Repositioning for Congenital Disorders of Glycosylation (CDG).

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