Synaptic dysfunction in Huntington's disease: a new perspective
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/213267
- author
- Smith, Ruben LU ; Brundin, Patrik LU and Li, Jia-Yi LU
- organization
- publishing date
- 2005
- type
- Contribution to journal
- 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
- 2022-04-23 01:54:10
@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}},
keywords = {{pathophysiology; neurotransmission; Huntington's disease; exocytosis; synaptic protein; endocytosis}},
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}},
}