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Huntingtons sjukdom - ännu ett galet protein?

Petersén, Åsa LU ; Hansson, Oskar LU orcid and Brundin, Patrik LU (2001) In Läkartidningen 98(50). p.5756-5761
Abstract
Huntington's disease is an autosomal dominant neurodegenerative disorder caused by an expanded CAG repeat. It is characterized by motor and cognitive disturbances, as well as cellular dysfunction and loss in the basal ganglia and the cerebral cortex. The mutant protein huntingtin aggregates in cells. The toxicity of mutant huntingtin, or the loss of its normal function, causes disruption of cellular functions such as protein and calcium metabolism, transmitter release, mitochondria and gene transcription. Recent findings in basic research open up new possibilities for novel therapies.
Please use this url to cite or link to this publication:
author
; and
organization
alternative title
[Huntington disease--yet another mad protein?]
publishing date
type
Contribution to journal
publication status
published
subject
in
Läkartidningen
volume
98
issue
50
pages
5756 - 5761
publisher
Swedish Medical Association
external identifiers
  • pmid:11789098
  • scopus:0035852392
ISSN
0023-7205
language
Swedish
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: Psychiatry/Primary Care/Public Health (013240500), Translational Neuroendocrinology (013210010), Neuronal Survival (013212041)
id
aa144377-39f2-4de7-932f-3ace1f67c1a5 (old id 1121170)
alternative location
http://ltarkiv.lakartidningen.se/artNo23918
date added to LUP
2016-04-01 16:20:45
date last changed
2022-01-28 19:01:24
@article{aa144377-39f2-4de7-932f-3ace1f67c1a5,
  abstract     = {{Huntington's disease is an autosomal dominant neurodegenerative disorder caused by an expanded CAG repeat. It is characterized by motor and cognitive disturbances, as well as cellular dysfunction and loss in the basal ganglia and the cerebral cortex. The mutant protein huntingtin aggregates in cells. The toxicity of mutant huntingtin, or the loss of its normal function, causes disruption of cellular functions such as protein and calcium metabolism, transmitter release, mitochondria and gene transcription. Recent findings in basic research open up new possibilities for novel therapies.}},
  author       = {{Petersén, Åsa and Hansson, Oskar and Brundin, Patrik}},
  issn         = {{0023-7205}},
  language     = {{swe}},
  number       = {{50}},
  pages        = {{5756--5761}},
  publisher    = {{Swedish Medical Association}},
  series       = {{Läkartidningen}},
  title        = {{Huntingtons sjukdom - ännu ett galet protein?}},
  url          = {{http://ltarkiv.lakartidningen.se/artNo23918}},
  volume       = {{98}},
  year         = {{2001}},
}