ORIGINAL ARTICLE

Potential role of α-synuclein in neurodegeneration: studies in a rat animal model

  1. George Stoica1,
  2. Gina Lungu1,
  3. Nicole L. Bjorklund2,
  4. Giulio Taglialatela2,
  5. Xing Zhang3,
  6. Veronica Chiu3,
  7. Herbert H. Hill3,
  8. James O. Schenk3,
  9. Ian Murray4

Article first published online: 22 JUN 2012

DOI: 10.1111/j.1471-4159.2012.07805.x

Issue

Journal of Neurochemistry

Journal of Neurochemistry

Volume 122, Issue 4, pages 812–822, August 2012

Additional Information

How to Cite

Stoica, G., Lungu, G., Bjorklund, N. L., Taglialatela, G., Zhang, X., Chiu, V., Hill, H. H., Schenk, J. O. and Murray, I. (2012), Potential role of α-synuclein in neurodegeneration: studies in a rat animal model. Journal of Neurochemistry, 122: 812–822. doi: 10.1111/j.1471-4159.2012.07805.x

Author Information

  1. 1

    Department of Veterinary Pathobiology, Texas A&M University, College Station, Texas, USA

  2. 2

    Department of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, Texas, USA

  3. 3

    Department of Chemistry, Washington State University, Pullman, Washington, USA

  4. 4

    Department of Neuroscience and Experimental Therapeutics Interdisciplinary Program in Neuroscience, Texas A&M University, College Station, Texas, USA

*Address correspondence and reprint requests to George Stoica DVM, PhD, Department of Veterinary Pathobiology, Texas A&M University, College Station, Texas 77843, USA. E-mail: gstoica@cvm.tamu.edu

Publication History

  1. Issue published online: 17 JUL 2012
  2. Article first published online: 22 JUN 2012
  3. Accepted manuscript online: 28 MAY 2012 08:35AM EST
  4. Received January 19, 2012; revised manuscript received May 14, 2012; accepted May 17, 2012.

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Keywords:

  • α-synuclein;
  • dopamine;
  • neurodegeneration;
  • Parkinson’s;
  • rat model

J. Neurochem. (2012) 122, 812–822.

Abstract

Neuronal protein α-synuclein (α-syn) is an essential player in the development of neurodegenerative diseases called synucleinopathies. A spontaneous autosomal recessive rat model for neurodegeneration was developed in our laboratory. These rats demonstrate progressive increases in α-syn in the brain mesencephalon followed by loss of dopaminergic terminals in the basal ganglia (BG) and motor impairments. The severity of pathology is directly related to the overexpression of α-syn and parallel decrease in dopamine (DA) level in the striatum (ST) of affected rats. The neurodegeneration in this model is characterized by the presence of perikarya and neurites Lewis bodies (LB) and diffuse marked accumulation of perikaryal α-syn in the substantia nigra (SN), brain stem (BS), and striatum (ST) along with neuronal loss. Light and ultrastructural analyses revealed that the process of neuronal degeneration is a ‘dying back’ type. The disease process is accompanied by gliosis and release of inflammatory cytokines. This neurodegeneration is a multisystemic disease and implicate α-syn as a major factor in the pathogenesis of this inherited autosomal recessive animal model. Decrease dopamine (DA) and overexpression of α-syn in the brain mesencephalon may provide a naturally occurring animal model for Parkinson’s disease (PD) and other synucleinopathies that reproduces significant pathological, neurochemical, and behavioral features of the human disease.

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