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Journal of Molecular Neuroscience

, Volume 24, Issue 3, pp 343–352 | Cite as

The role of α-synuclein assembly and metabolism in the pathogenesis of Lewy body disease

  • Makoto Hashimoto
  • Kohichi Kawahara
  • Pazit Bar-On
  • Edward Rockenstein
  • Leslie Crews
  • Eliezer Masliah
Original Article

Abstract

Parkinson’s disease (PD) and dementia with Lewy bodies (DLB) are members of a family of disorders characterized by the presence of inclusion bodies, or Lewy bodies (LBs), filled with aggregates of α-synuclein. These diseases are a leading cause of movement disorders and dementia in the aging population, and it is crucial to understand the factors leading to the accumulation and assembly of these α-synuclein aggregates. Previous studies have uncovered much about the factors leading to aggregation and the mechanisms causing neurotoxicity of these inclusion bodies; however, little is known about factors that promote the degradation and prevent the aggregation of α-synuclein. The present article provides a review of recent efforts in the investigation of factors involved in α-synuclein metabolism and the mechanisms involved in preventing accumulation of α-synuclein and degrading this molecule. Understanding these processes might provide targets for the development of novel therapies for disorders such as DLB and PD.

Index Entries

α-synuclein degradation metabolism Lewy bodies proteasom ubiquitin 

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Copyright information

© Humana Press Inc 2004

Authors and Affiliations

  • Makoto Hashimoto
    • 1
  • Kohichi Kawahara
    • 1
  • Pazit Bar-On
    • 1
  • Edward Rockenstein
    • 1
  • Leslie Crews
    • 1
  • Eliezer Masliah
    • 1
    • 2
  1. 1.Department of NeurosciencesUniversity of California San DiegoLa Jolla
  2. 2.Department of PathologyUniversity of California San DiegoLa Jolla

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