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Synaptic dysfunction in Huntington's disease: a new perspective

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Author

Summary, in English

Huntington's disease (HD) is caused by a polyglutamine expansion in the protein huntingtin and is characterized by intraneuronal inclusions and widespread neuronal death at the late stage of the disease. In research, most of the emphasis has been on understanding the cell death and its mechanisms. Until recently, it was believed that the vast majority, if not all, of the symptoms in HD are a direct consequence of neurodegeneration. However, increasing evidence shows that subtle alterations in synaptic function could underlie the early symptoms. It is of particular interest to understand the nature of this neuronal dysfunction. Normal huntingtin interacts with various cytoskeletal and synaptic vesicle proteins that are essential for exocytosis and endocytosis. Altered interactions of mutant huntingtin with its associated partners could contribute to abnormal synaptic transmission in HD. This review describes recent advances in understanding synaptic dysfunction in HD.

Publishing year

2005

Language

English

Pages

1901-1912

Publication/Series

Cellular and Molecular Life Sciences

Volume

62

Issue

17

Document type

Journal article review

Publisher

Birkhäuser Verlag

Topic

  • Cell Biology

Keywords

  • pathophysiology
  • neurotransmission
  • Huntington's disease
  • exocytosis
  • synaptic protein
  • endocytosis

Status

Published

ISBN/ISSN/Other

  • ISSN: 1420-9071