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Hypothalamic and Neuroendocrine Changes in Huntington's Disease.

Hult Lundh, Sofia LU ; Schultz, Kristofer LU ; Soylu, Rana LU and Petersén, Åsa LU (2010) In Current drug targets 11. p.1237-1249
Abstract
Huntington's disease (HD) is a fatal hereditary neurodegenerative disorder without satisfactory treatments nor a cure. It is caused by a CAG repeat expansion in the huntingtin gene. The clinical symptoms involve motor-, cognitive- and psychiatric disturbances. Recent studies have shown that non-motor symptoms and signs, such as mood changes, sleep disturbances and metabolic alterations often occur before the onset of overt motor impairments. The hypothalamus is one of the main regulators of emotion, sleep and metabolism, and it is therefore possible that dysfunction of the hypothalamus and neuroendocrine circuits may, at least partly, be responsible for these non-motor symptoms in HD. Several hypothalamic and neuroendocrine changes have... (More)
Huntington's disease (HD) is a fatal hereditary neurodegenerative disorder without satisfactory treatments nor a cure. It is caused by a CAG repeat expansion in the huntingtin gene. The clinical symptoms involve motor-, cognitive- and psychiatric disturbances. Recent studies have shown that non-motor symptoms and signs, such as mood changes, sleep disturbances and metabolic alterations often occur before the onset of overt motor impairments. The hypothalamus is one of the main regulators of emotion, sleep and metabolism, and it is therefore possible that dysfunction of the hypothalamus and neuroendocrine circuits may, at least partly, be responsible for these non-motor symptoms in HD. Several hypothalamic and neuroendocrine changes have now been identified in clinical HD as well as in rodent models of the disease. These changes could be important both in the pathogenesis of HD, constitute biomarkers to track disease progression as well as to provide novel therapeutic targets for this devastating disease. The current state of knowledge in the area of hypothalamic and neuroendocrine changes in both patients and rodent models of HD is summarized in this review, and their potential as targets for novel treatment paradigms are discussed. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Current drug targets
volume
11
pages
1237 - 1249
publisher
Bentham Science Publishers
external identifiers
  • WOS:000285183900005
  • PMID:20594177
ISSN
1873-5592
language
English
LU publication?
yes
id
64f5615b-de67-4e44-aeaf-4414d7b403fa (old id 1645356)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/20594177?dopt=Abstract
date added to LUP
2010-08-02 09:32:00
date last changed
2016-04-16 06:56:40
@article{64f5615b-de67-4e44-aeaf-4414d7b403fa,
  abstract     = {Huntington's disease (HD) is a fatal hereditary neurodegenerative disorder without satisfactory treatments nor a cure. It is caused by a CAG repeat expansion in the huntingtin gene. The clinical symptoms involve motor-, cognitive- and psychiatric disturbances. Recent studies have shown that non-motor symptoms and signs, such as mood changes, sleep disturbances and metabolic alterations often occur before the onset of overt motor impairments. The hypothalamus is one of the main regulators of emotion, sleep and metabolism, and it is therefore possible that dysfunction of the hypothalamus and neuroendocrine circuits may, at least partly, be responsible for these non-motor symptoms in HD. Several hypothalamic and neuroendocrine changes have now been identified in clinical HD as well as in rodent models of the disease. These changes could be important both in the pathogenesis of HD, constitute biomarkers to track disease progression as well as to provide novel therapeutic targets for this devastating disease. The current state of knowledge in the area of hypothalamic and neuroendocrine changes in both patients and rodent models of HD is summarized in this review, and their potential as targets for novel treatment paradigms are discussed.},
  author       = {Hult Lundh, Sofia and Schultz, Kristofer and Soylu, Rana and Petersén, Åsa},
  issn         = {1873-5592},
  language     = {eng},
  pages        = {1237--1249},
  publisher    = {Bentham Science Publishers},
  series       = {Current drug targets},
  title        = {Hypothalamic and Neuroendocrine Changes in Huntington's Disease.},
  volume       = {11},
  year         = {2010},
}