Serum dehydroepiandrosterone and cortisol measurements in Huntington's chorea

Leblhuber, Friedrich; Peichl, Marianne; Neubauer, C.; Reisecker, F; Steinparz, F.X.; Windhager, Elmar; Maschek, W

doi:10.1016/0022-510x(95)00114-h

Cited by 54 publications

(39 citation statements)

References 30 publications

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“…HD may be associated with inflammatory changes in the brain (Bonifati & Kishore 2007), as well as physiological stress responses that may be intrinsic to the disease, or caused by perception of symptoms (e.g. Leblhuber et al 1995;Petersen & Bjorkqvist 2006). Either or both may have played a role in the elevated levels of APP observed, indicating reduced welfare in the HD mice.…”

Section: Discussion (A) Disease Progression In Se and Re Cagesmentioning

confidence: 99%

Towards humane end points: behavioural changes precede clinical signs of disease in a Huntington's disease model

et al. 2008

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The number of animals used in science is increasing, bringing a concomitant obligation to minimize suffering. For animals with progressive conditions, euthanasia at a 'humane end point' is advised if the end point is scientifically valid, predictive and accurate. Our aim was to test the hypothesis that behavioural changes would reliably precede clinical signs of disease in a progressive neurological model, using retrospective analysis. We observed 100 pair-housed female R6/1 transgenic Huntington's disease (HD) mice and 28 pair-housed female wild-type (WT) mice in standard-or resource-enriched cages. Disease progression was monitored until one member of each HD pair reached a pre-defined end point based on pathological symptoms (HD end). This mouse was then euthanized together with its cage mate (HD other) and any matched WT pairs. At euthanasia, HD mice had significantly greater absolute and relative organ weights, and significantly higher a1 acid glycoprotein concentrations than WT mice, indicating reduced welfare. HD mice initially showed significantly greater use of cage resources than WT mice but this declined progressively. Steeper declines, and earlier cessation, in the use of some climbing and exploration resources occurred in the HD end mice compared with the HD other mice. Behavioural change can be an early indicator of disease onset.

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Section: Discussion (A) Disease Progression In Se and Re Cagesmentioning

confidence: 99%

Towards humane end points: behavioural changes precede clinical signs of disease in a Huntington's disease model

et al. 2008

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“…Hypothalamic degeneration, including neuronal loss in specific sub-nuclei, has been documented >15 years before predicted clinical onset [26][27][28] , and results in hypothalamicpituitary-adrenal (HPA) axis dysregulation, producing circadian rhythm disturbances and metabolic imbalances unfavourably impacting on homeostasis and body weight 17,[29][30][31][32][33][34][35][36][37][38][39][40][41] .…”

Section: List Of Figuresmentioning

confidence: 99%

“…Patients with Huntington's disease may experience elevated cortisol levels 29,31,35,41,119 and progressive increases in cortisol have been noted in Huntington's disease animal models 30 . Exercise has been shown to affect cortisol levels in humans, although this response is mediated by factors including the type of exercise, intensity of exercise and diurnal rhythm [120][121][122][123] .…”

Section: D-kefs Trail Makingmentioning

confidence: 99%

First use of creatine hydrochloride in premanifest Huntington disease

Tuckfield

2015

Medical Journal of Australia

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“…Increased CRF levels have been found in the cerebrospinal fluid from patients with early HD [102] . Increased cortisol and vasopressin levels have been found in plasma and urine in clinical HD [86,96,103,104] . Ongoing studies in different laboratories are now examining these changes in further detail.…”

Section: Alterations In the Hypothalamic-pituitary-adrenal Axismentioning

confidence: 99%

Huntington’s Disease – New Perspectives Based on Neuroendocrine Changes in Rodent Models

Petersén¹,

Hult²,

Kirik³

2009

Neurodegener Dis

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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.

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Serum dehydroepiandrosterone and cortisol measurements in Huntington's chorea

Cited by 54 publications

References 30 publications

Towards humane end points: behavioural changes precede clinical signs of disease in a Huntington's disease model

Towards humane end points: behavioural changes precede clinical signs of disease in a Huntington's disease model

First use of creatine hydrochloride in premanifest Huntington disease

Huntington’s Disease – New Perspectives Based on Neuroendocrine Changes in Rodent Models

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