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Interaction Study of Antioxidants with Progressive Myoclonus Epilepsy by Molecular Docking Techniques


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1 Amity Institute of Biotechnology, Amity University, Lucknow, UP- 226028, India
     

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Progressive Myoclonus Epilepsy (PME) is a rare epilepsy syndrome caused by number of genetic disorders .This syndrome contains myoclonic seizures and chronic seizures along with progressive neurological decline. Oxidative stress can result into mild or severe form of these diseases and remain the cause of several other diseases such as cardiovascular diseases, neurological diseases, malignancies, renal disease, diabetes, inflammatory, skin diseases, aging, respiratory diseases, liver diseases, and different type of viral infection. The evaluation of the effectiveness of various, antioxidants is being targeted due to clinical, trials of several neurodegenerative diseases. In this study we have seen the effectiveness of antioxidants against Progressive Myoclonus Epilepsy disease .Docking is done using Schrödinger software, interaction studies shows that Resveratrol is potential drug against myoclonus epilepsy. Further study shows that antioxidants can be better inhibitor of myoclonus epilepsy disease.

Keywords

Lafora Disease, Antioxidants, Resveratrol, Schrödinger Software, Docking.
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  • Girard, Jean-Marie, et al. "Progressive myoclonus epilepsy." Handbook of clinical neurology. Vol. 113. Elsevier, 2013. 1731-1736.
  • Zupanc, Mary L., and Benjamin Legros. "Progressive myoclonic epilepsy." The Cerebellum 3.3 (2004): 156.
  • Satishchandra, P., and S. Sinha. "Progressive myoclonic epilepsy." Neurology India 58.4 (2010): 514.
  • Pennacchio, Len A., et al. "Mutations in the gene encoding cystatin B in progressive myoclonus epilepsy (EPM1)." Science 271.5256 (1996): 1731-1734.
  • Chan, Elayne M., et al. "Mutations in NHLRC1 cause progressive myoclonus epilepsy." Nature genetics 35.2 (2003): 125.
  • Vilchez, David, et al. "Mechanism suppressing glycogen synthesis in neurons and its demise in progressive myoclonus epilepsy." Nature neuroscience 10.11 (2007): 1407.
  • Berkovic, Samuel F., et al. "Progressive myoclonus epilepsies: specific causes and diagnosis." New England Journal of Medicine 315.5 (1986): 296-305.
  • Ganesh, Subramaniam, et al. "Recent advances in the molecular basis of Lafora’s progressive myoclonus epilepsy." Journal of human genetics 51.1 (2006): 1-8.
  • Minassian, Berge A., et al. "Mutations in a gene encoding a novel protein tyrosine phosphatase cause progressive myoclonus epilepsy." Nature genetics 20.2 (1998): 171.
  • Singh, Shweta, and Subramaniam Ganesh. "Lafora progressive myoclonus epilepsy: A meta‐analysis of reported mutations in the first decade following the discovery of the EPM2A and NHLRC1 genes." Human mutation 30.5 (2009): 715-723.
  • Delgado-Escueta, Antonio V. "Advances in lafora progressive myoclonus epilepsy." Current neurology and neuroscience reports 7.5 (2007): 428-433.
  • Chan, E. M., et al. "Genetic mapping of a new Lafora progressive myoclonus epilepsy locus (EPM2B) on 6p22." Journal of medical genetics 40.9 (2003): 671-675.
  • Vilchez, David, et al. "Mechanism suppressing glycogen synthesis in neurons and its demise in progressive myoclonus epilepsy." Nature neuroscience 10.11 (2007): 1407.
  • Ianzano, Leonarda, et al. "Lafora progressive myoclonus epilepsy mutation database‐EPM2A and NHLRC1 (EMP2B) genes." Human mutation 26.4 (2005): 397-397.
  • Chan, E. M., et al. "Progressive myoclonus epilepsy with polyglucosans (Lafora disease) Evidence for a third locus." Neurology 63.3 (2004): 565-567.
  • Pennacchio, Len A., et al. "Mutations in the gene encoding cystatin B in progressive myoclonus epilepsy (EPM1)." Science 271.5256 (1996): 1731-1734.
  • Minassian, Berge A., et al. "Mutations in a gene encoding a novel protein tyrosine phosphatase cause progressive myoclonus epilepsy." Nature genetics 20.2 (1998): 171.
  • Berman, Helen, et al. "The worldwide Protein Data Bank (wwPDB): ensuring a single, uniform archive of PDB data." Nucleic acids research 35.suppl_1 (2006): D301-D303.
  • Butkiewicz, Mariusz, et al. "Benchmarking ligand-based virtual High-Throughput Screening with the PubChem database." Molecules 18.1 (2013): 735-756.
  • Schrodinger, L. "Schrodinger software suite." New York: Schrödinger, LLC 670 (2011).
  • Halgren, Thomas A., et al. "Glide: a new approach for rapid, accurate docking and scoring. 2. Enrichment factors in database screening." Journal of medicinal chemistry 47.7 (2004): 1750-1759.
  • Tian, Ye, Xu Han, and Da‐li Tian. "The biological regulation of ABCE1." IUBMB life 64.10 (2012): 795-800.
  • Alonso, Andres, et al. "Protein tyrosine phosphatases in the human genome." Cell 117.6 (2004): 699-711.
  • Malaspina, Andrea, Narendra Kaushik, and Jackie De Belleroche. "Differential expression of 14 genes in amyotrophic lateral sclerosis spinal cord detected using gridded cDNA arrays." Journal of neurochemistry 77.1 (2001): 132-145.
  • Bountra, Chas, Udo Oppermann, and Tom D. Heightman. "Animal models of epigenetic regulation in neuropsychiatric disorders." Molecular and Functional Models in Neuropsychiatry. Springer, Berlin, Heidelberg, 2011. 281-322.

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  • Interaction Study of Antioxidants with Progressive Myoclonus Epilepsy by Molecular Docking Techniques

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Authors

Ruchi Yadav
Amity Institute of Biotechnology, Amity University, Lucknow, UP- 226028, India
Prachi Srivastava
Amity Institute of Biotechnology, Amity University, Lucknow, UP- 226028, India

Abstract


Progressive Myoclonus Epilepsy (PME) is a rare epilepsy syndrome caused by number of genetic disorders .This syndrome contains myoclonic seizures and chronic seizures along with progressive neurological decline. Oxidative stress can result into mild or severe form of these diseases and remain the cause of several other diseases such as cardiovascular diseases, neurological diseases, malignancies, renal disease, diabetes, inflammatory, skin diseases, aging, respiratory diseases, liver diseases, and different type of viral infection. The evaluation of the effectiveness of various, antioxidants is being targeted due to clinical, trials of several neurodegenerative diseases. In this study we have seen the effectiveness of antioxidants against Progressive Myoclonus Epilepsy disease .Docking is done using Schrödinger software, interaction studies shows that Resveratrol is potential drug against myoclonus epilepsy. Further study shows that antioxidants can be better inhibitor of myoclonus epilepsy disease.

Keywords


Lafora Disease, Antioxidants, Resveratrol, Schrödinger Software, Docking.

References