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Analysis of the possible involvement of the glutamate transporter gene EAAT2 and the glutamate receptor genes GRIA1 and GRIA2 in the pathogenesis of motor neuron disease in the Russian population

  • Human Genetics
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Abstract

Polymorphisms of the genes of the glutamatergic system EAAT2, GRIA1, and GRIA2 have been analyzed in patients with sporadic motor neuron disease (MND) from Russia. The disease is not associated with polymorphic alleles of the genes studied, which indicates that EAAT2, GRIA1, and GRIA2 play an insignificant role in the pathogenesis of sporadic MND.

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References

  1. Skvortsova, V., Shadrina, M., Slominsky, P., et al., Analysis of Heavy Neurofilament Subunit Gene Polymorphism in Russian Patients with Sporadic Motor Neuron Disease (MND), Eur. J. Hum. Genet., 2004, vol. 12, pp. 241–244.

    Article  CAS  PubMed  Google Scholar 

  2. Zherebtsova, A.L., Shadrina, M.I., Levitsky, G.N., et al., Analysis of the Glutathione S-Transferase P1 Gene Ile105Val Polymorphism in the Patients with Sporadic Motor Neuron Disease from Russia, Rus. J. Genet., 2004, vol. 40, no. 6, pp. 691–693.

    Article  CAS  Google Scholar 

  3. Kondratyeva, E.A., Shadrina, M.I., Levitsky, G.N., et al., Analysis of the Ala9Val Polymorphism of the MnContaining Superdismutase Gene in Patients with Sporadic Motor Neuron Disease from Russia, Med. Genet., 2003, vol. 2, no. 9, pp. 442–444.

    Google Scholar 

  4. Shadrina, M.I., Kondratyeva, E.A., Slominsky, P.A., et al., Polymorphism of Glutathione S-Transferase Genes M1 and T1 in Patients with Motor Neuron Disease from the Moscow Population, Rus. J. Genet., 2002, vol. 38, no. 11, pp. 1327–1329.

    Article  CAS  Google Scholar 

  5. Shadrina, M.I., Slominsky, P.A., Levitsky, G.N., et al., Sporadic Amyotriphic Lateral Sclerosis: Analysis of Genetic Risk Factors in the Russian Population, Med. Genet., 2004, vol. 3, no. 11, pp. 513–520.

    CAS  Google Scholar 

  6. Skvortsova, V.I., Limborska, S.A., Slominsky, P.A., et al., Sporadic ALS Associated with the D90A Cu,Zn Superoxide Dismutase Mutation in Russia, Eur. J. Neurol., 2001, vol. 8, pp. 167–172.

    Article  CAS  PubMed  Google Scholar 

  7. Zavalishin, I. and Zakharova, M., Amyotrophic Lateral Sclerosis, Zh. Nevrol. Psikhiatr., 1999, vol. 99, no. 4, pp. 60–64.

    CAS  Google Scholar 

  8. Gregor, P., Reeves, R., Jabs, E., et al., Chromosomal Localization of Glutamate Receptor Genes: Relationship to Familial Amyotrophic Lateral Sclerosis and Other Neurological Disorders of Mice and Humans, Proc. Natl. Acad. Sci. USA: Neurobiology, 1993, vol. 90, pp. 3053–3057.

    CAS  Google Scholar 

  9. Harrison, P.J., Law, A.J., and Eastwood, S.L., Glutamate and Transporters in the Hippocampus in Schizophrenia, Ann. N. Y. Acad. Sci., 2003, no. 1003, pp. 94–101.

  10. Ludolph, A.C., Meyer, T., and Riepe, M.W., The Role of Excitotoxicity in ALS—What Is the Evidence?, J. Neurol., 2000, vol. 247, pp. 7–16.

    Article  Google Scholar 

  11. Otis, T.S., Brasnjo, G., Dzubay, J.A., and Pratap, M., Interactions between Glutamate Transporters and Metabotropic Glutamate Receptors at Excitatory Synapses in the Cerebellar Cortex, Neurochem. Int., 2003, vol. 45, pp. 537–544.

    Google Scholar 

  12. Sander, T., Berlin, W., Ostapowicz, A., et al., Variation of the Genes Encoding the Human Glutamate EAAT2, Serotonin and Dopamine Transporters and Susceptibility to Idiopathic Generalized Epilepsy, Epilepsy Res., 2000, vol. 41, pp. 75–81.

    Article  CAS  PubMed  Google Scholar 

  13. Semyanov, A. and Kullmann, D.M., Kainate Receptor-Dependent Axonal Depolarization and Action Potential Initiation in Interneurons, Nat. Neurosci., 2001, vol. 4, no. 7, pp. 718–723.

    Article  CAS  PubMed  Google Scholar 

  14. Tsai, S., Liu, H., Liu, T., et al., Association Analysis for the Genetic Variants of the NMDA Receptor Subunit 2b Alzheimer’s Disease, Dement. Geriatr. Cogn. Disord., 2002, vol. 13, pp. 91–94.

    Article  CAS  PubMed  Google Scholar 

  15. Howland, D.S., Liu, J., She, Y., et al., Focal Loss of the Glutamate Transporter EAAT2 in a Transgenic Rat Model of SOD1 Mutant-Mediated Amyotrophic Lateral Sclerosis (ALS), Proc. Natl. Acad. Sci. USA: Neurobiology, 2002, vol. 99, no. 3, pp. 1604–1609.

    CAS  Google Scholar 

  16. Trotti, D., Aoki, M., Pasinelli, P., et al., Amyotrophic Lateral Sclerosis-Linked Glutamate Transporter Mutant Has Impaired Glutamate Clearance Capacity, J. Biol. Chem., 2001, vol. 276, no. 1, pp. 576–582.

    CAS  PubMed  Google Scholar 

  17. Su, Z., Leszczyniecka, M., Kang, D., et al., Insights into Glutamate Transport Regulation in Human Astrocytes: Cloning of the Promoter for Excitatory Amino Acid Transporter 2 (EAAT2), Proc. Natl. Acad. Sci. USA, 2003, vol. 100, pp. 1955–1960.

    CAS  PubMed  Google Scholar 

  18. Jackson, M., Steers, G., Leigh, P., and Morrison, K., Polymorphisms in the Glutamate Transporter Gene EAAT2 in European ALS Patients, J. Neurol., 1999, vol. 246, pp. 1140–1144.

    Article  CAS  PubMed  Google Scholar 

  19. Aoki, M., Lin, C., Rothstein, J., et al., Mutations in the Glutamate Transporter EAAT2 Gene Do Not Cause Abnormal EAAT2 Transcripts in Amyotrophic Lateral Sclerosis, Ann. Neurol., 1998, vol. 43, pp. 645–653.

    Article  CAS  PubMed  Google Scholar 

  20. Hillel, A.D., Miller, R.M., Yorkston, K., et al., Amyotrophic Lateral Sclerosis Severity Scale, Neuroepidemiology, 1989, vol. 8, no. 3, pp. 142–150.

    CAS  PubMed  Google Scholar 

  21. Sambrook, J., Fritsch, E.F., and Maniatis, T., Molecular Cloning: A Laboratory Manual, Cold Spring Harbor, New York Cold Spring Harbor Lab., 1989.

    Google Scholar 

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Authors and Affiliations

  1. Institute of Molecular Genetics, Russian Academy of Sciences, Moscow, 123182, Russia

    A. L. Zherebtsova, M. I. Shadrina, E. V. Semenova, P. A. Slominsky & S. A. Limborska

  2. Russian State Medical University, Moscow, 129327, Russia

    G. N. Levitsky, A. V. Alekhin & V. I. Skvortsova

Authors
  1. A. L. Zherebtsova
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  2. M. I. Shadrina
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  3. E. V. Semenova
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  4. G. N. Levitsky
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  5. A. V. Alekhin
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  6. P. A. Slominsky
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  7. V. I. Skvortsova
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  8. S. A. Limborska
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Additional information

Original Russian Text © A.L. Zherebtsova, M.I. Shadrina, E.V. Semenova, G.N. Levitsky, A.V. Alekhin, PA. Slominsky, V.I. Skvortsova, S.A. Limborska, 2006, published in Genetika, 2006, Vol. 42, No. 1, pp. 104–109.

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Zherebtsova, A.L., Shadrina, M.I., Semenova, E.V. et al. Analysis of the possible involvement of the glutamate transporter gene EAAT2 and the glutamate receptor genes GRIA1 and GRIA2 in the pathogenesis of motor neuron disease in the Russian population. Russ J Genet 42, 89–93 (2006). https://doi.org/10.1134/S1022795406010133

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  • DOI: https://doi.org/10.1134/S1022795406010133

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