Huntington's Disease - New Perspectives Based on Neuroendocrine Changes in Rodent Models.
(2009) In Neurodegenerative Diseases 6. p.154-164- Abstract
- Huntington's disease (HD) is a neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin gene. Although it is characterized by progressive motor impairments, cognitive changes and psychiatric disturbances are major components of the disease. In addition, recent studies have shown that other non-motor symptoms such as alterations in sleep pattern, disruption of the circadian rhythm and increased energy metabolism are common and occur early. Emerging evidence suggests that the latter symptoms are likely results of disturbed functions of the hypothalamus and neuroendocrine circuits, which are known to be central in the regulation of emotion, sleep and metabolism. Whereas clinical data are essential to define key... (More)
- Huntington's disease (HD) is a neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin gene. Although it is characterized by progressive motor impairments, cognitive changes and psychiatric disturbances are major components of the disease. In addition, recent studies have shown that other non-motor symptoms such as alterations in sleep pattern, disruption of the circadian rhythm and increased energy metabolism are common and occur early. Emerging evidence suggests that the latter symptoms are likely results of disturbed functions of the hypothalamus and neuroendocrine circuits, which are known to be central in the regulation of emotion, sleep and metabolism. Whereas clinical data are essential to define key pathological features of HD, animal models that can recapitulate the neurobiological and behavioral features of the disorder are critical tools to elucidate the underlying pathogenic mechanisms. Recent studies employing different HD rodent models have been instrumental in identifying a number of neuroendocrine alterations as well as in highlighting novel potential disease pathways. This review summarizes the current state of knowledge derived from neuroendocrine studies in rodent models of HD in light of clinical relevance and points to future implications for this emerging field. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1434290
- author
- Petersén, Åsa LU ; Hult Lundh, Sofia LU and Kirik, Deniz LU
- organization
- publishing date
- 2009
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Neurodegenerative Diseases
- volume
- 6
- pages
- 154 - 164
- publisher
- Karger
- external identifiers
-
- wos:000269623400003
- pmid:19521064
- scopus:69249212206
- pmid:19521064
- ISSN
- 1660-2862
- DOI
- 10.1159/000225377
- language
- English
- LU publication?
- yes
- id
- 8062eb6d-3f9d-4a31-a5a6-513bf67a78b3 (old id 1434290)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/19521064?dopt=Abstract
- date added to LUP
- 2016-04-04 07:07:34
- date last changed
- 2022-01-29 01:44:11
@article{8062eb6d-3f9d-4a31-a5a6-513bf67a78b3,
abstract = {{Huntington's disease (HD) is a neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin gene. Although it is characterized by progressive motor impairments, cognitive changes and psychiatric disturbances are major components of the disease. In addition, recent studies have shown that other non-motor symptoms such as alterations in sleep pattern, disruption of the circadian rhythm and increased energy metabolism are common and occur early. Emerging evidence suggests that the latter symptoms are likely results of disturbed functions of the hypothalamus and neuroendocrine circuits, which are known to be central in the regulation of emotion, sleep and metabolism. Whereas clinical data are essential to define key pathological features of HD, animal models that can recapitulate the neurobiological and behavioral features of the disorder are critical tools to elucidate the underlying pathogenic mechanisms. Recent studies employing different HD rodent models have been instrumental in identifying a number of neuroendocrine alterations as well as in highlighting novel potential disease pathways. This review summarizes the current state of knowledge derived from neuroendocrine studies in rodent models of HD in light of clinical relevance and points to future implications for this emerging field.}},
author = {{Petersén, Åsa and Hult Lundh, Sofia and Kirik, Deniz}},
issn = {{1660-2862}},
language = {{eng}},
pages = {{154--164}},
publisher = {{Karger}},
series = {{Neurodegenerative Diseases}},
title = {{Huntington's Disease - New Perspectives Based on Neuroendocrine Changes in Rodent Models.}},
url = {{http://dx.doi.org/10.1159/000225377}},
doi = {{10.1159/000225377}},
volume = {{6}},
year = {{2009}},
}