Neuroendocrine and neurotrophic signaling in Huntington’s disease: Implications for pathogenic mechanisms and treatment strategies

Danielle M. Bartlett; Travis M. Cruickshank; Anthony J. Hannan; Peter R. Eastwood; Alpar S. Lazar; Mel R. Ziman

doi:10.1016/j.neubiorev.2016.09.006

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Neuroendocrine and neurotrophic signaling in Huntington’s disease: Implications for pathogenic mechanisms and treatment strategies

Journal article

Open access

Peer reviewed

Neuroendocrine and neurotrophic signaling in Huntington’s disease: Implications for pathogenic mechanisms and treatment strategies

Danielle M. Bartlett, Travis M. Cruickshank, Anthony J. Hannan, Peter R. Eastwood, Alpar S. Lazar and Mel R. Ziman

Neuroscience and biobehavioral reviews, Vol.71, pp.444-454

2016

DOI: https://doi.org/10.1016/j.neubiorev.2016.09.006

PMID: 27637496

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Abstract

Brain-derived neurotrophic factor (BDNF)

Circadian rhythm

Hypothalamic-pituitary-adrenal (HPA) axis

Hypothalamus

Sleep

Suprachiasmatic nucleus (SCN)

Huntington’s disease (HD) is a fatal neurodegenerative disease caused by an extended polyglutamine tract in the huntingtin protein. Circadian, sleep and hypothalamic-pituitary-adrenal (HPA) axis disturbances are observed in HD as early as 15 years before clinical disease onset. Disturbances in these key processes result in increased cortisol and altered melatonin release which may negatively impact on brain-derived neurotrophic factor (BDNF) expression and contribute to documented neuropathological and clinical disease features. This review describes the normal interactions between neurotrophic factors, the HPA-axis and circadian rhythm, as indicated by levels of BDNF, cortisol and melatonin, and the alterations in these intricately balanced networks in HD. We also discuss the implications of these alterations on the neurobiology of HD and the potential to result in hypothalamic, circadian, and sleep pathologies. Measurable alterations in these pathways provide targets that, if treated early, may reduce degeneration of brain structures. We therefore focus here on the means by which multidisciplinary therapy could be utilised as a non-pharmaceutical approach to restore the balance of these pathways.

Details

Title: Neuroendocrine and neurotrophic signaling in Huntington’s disease: Implications for pathogenic mechanisms and treatment strategies
Authors/Creators: Danielle M. Bartlett - Edith Cowan University
Travis M. Cruickshank - Edith Cowan University
Anthony J. Hannan - Florey Institute of Neuroscience and Mental Health
Peter R. Eastwood - The University of Western Australia
Alpar S. Lazar - University of Cambridge
Mel R. Ziman - School of Medical and Health Sciences, Edith Cowan University, 270 Joondalup Drive, Perth, Australia
Publication Details: Neuroscience and biobehavioral reviews, Vol.71, pp.444-454
Publisher: Elsevier Ltd
Identifiers: 991005592645307891
Murdoch Affiliation: Vice Chancellery
Language: English
Resource Type: Journal article

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Collaboration types: Domestic collaboration; International collaboration
Citation topics: 1 Clinical & Life Sciences; 1.52 Neurodegenerative Diseases; 1.52.951 Huntington's and Ataxias
Web Of Science research areas: Behavioral Sciences; Neurosciences
ESI research areas: Neuroscience & Behavior