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

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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.

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Authors and Affiliations

  1. Department of Neurosciences, University of California San Diego, 92093-0624, La Jolla, CA

    Makoto Hashimoto, Kohichi Kawahara, Pazit Bar-On, Edward Rockenstein, Leslie Crews & Eliezer Masliah

  2. Department of Pathology, University of California San Diego, 92093-0624, La Jolla, CA

    Eliezer Masliah

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  1. Makoto Hashimoto
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  2. Kohichi Kawahara
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  3. Pazit Bar-On
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  4. Edward Rockenstein
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  5. Leslie Crews
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  6. Eliezer Masliah
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Correspondence to Eliezer Masliah.

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Hashimoto, M., Kawahara, K., Bar-On, P. et al. The role of α-synuclein assembly and metabolism in the pathogenesis of Lewy body disease. J Mol Neurosci 24, 343–352 (2004). https://doi.org/10.1385/JMN:24:3:343

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