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

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