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Synaptic dysfunction in Huntington's disease: a new perspective

Smith, Ruben LU ; Brundin, Patrik LU and Li, Jia-Yi LU (2005) In Cellular and Molecular Life Sciences 62(17). p.1901-1912
Abstract
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... (More)
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. (Less)
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author
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organization
publishing date
type
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publication status
published
subject
keywords
pathophysiology, neurotransmission, Huntington's disease, exocytosis, synaptic protein, endocytosis
in
Cellular and Molecular Life Sciences
volume
62
issue
17
pages
1901 - 1912
publisher
Birkhäuser Verlag
external identifiers
  • wos:000232497400001
  • scopus:24344461460
ISSN
1420-9071
DOI
10.1007/s00018-005-5084-5
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Neuronal Survival (013212041)
id
3292af63-62f4-48a3-9945-e86e69921aa9 (old id 213267)
date added to LUP
2016-04-01 16:59:21
date last changed
2020-12-01 01:36:40
@article{3292af63-62f4-48a3-9945-e86e69921aa9,
  abstract     = {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.},
  author       = {Smith, Ruben and Brundin, Patrik and Li, Jia-Yi},
  issn         = {1420-9071},
  language     = {eng},
  number       = {17},
  pages        = {1901--1912},
  publisher    = {Birkhäuser Verlag},
  series       = {Cellular and Molecular Life Sciences},
  title        = {Synaptic dysfunction in Huntington's disease: a new perspective},
  url          = {http://dx.doi.org/10.1007/s00018-005-5084-5},
  doi          = {10.1007/s00018-005-5084-5},
  volume       = {62},
  year         = {2005},
}