This study was reported in the Journal of Huntington’s Disease (JHD).
HD is an autosomal-dominant hereditary neurodegenerative condition, characterized by a triad of motor, cognitive, and psychiatric features resulting from a polyglutamine expansion mutation in exon 1 of the huntingtin gene. Because there is currently no treatment that slows or halts the progression of the disease, contemporary treatment approaches to address symptoms. Sleep dysfunction represents one such highly prevalent symptom.
Disrupted sleep can alter metabolism and increases vulnerability to infection. Many of us have experienced the increased irritability, sluggish thinking, and physical exhaustion that comes with a poor night’s sleep. There is an emerging awareness that both sleep and circadian rhythm abnormalities are associated with neurodegenerative diseases.
Prof. Morton continues: “It is clear from the articles in this special issue that sleep and circadian dysfunction in HD patients is an understudied, indeed neglected, field. Yet a lack of study is not the only issue. The lack of recognition of the problem is as great a barrier to progress. Sleep dysfunction in normal people is taken seriously, and it is recognized that it exacerbates a range of cognitive symptoms, including deficits in executive function, memory consolidation, attention, and processing speed, as well as affective features such as impulsivity and emotional liability. Notably, most if not all these symptoms are present in HD at some stage in the course of the disease, yet the impact of sleep dysfunction on HD patient symptoms is rarely considered.”
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There is growing evidence from both clinical and animal model studies that sleep changes occur early in the clinical course of the disease. Difficulties with sleep initiation and maintenance that lead not only to decreased sleep efficiency but also to progressive deterioration of normal sleep architecture are recognized as symptoms of HD. Sleep alterations in HD are under-reported by patients and unrecognized by health professionals. This may explain why available investigations of sleep in HD patients are sparse, with small cohorts, and varying methodologies.
Sleep disruption may not only exacerbate cognitive and affective symptoms but also directly affect neurodegenerative processes by inducing neuroinflammation or impairing slow-wave sleep-dependent glymphatic clearance of neurotoxic waste. If sleep deprivation is associated with an increase in neurotoxic proteins such as b-amyloid and tau, known contributors to neurodegeneration in Alzheimer’s disease, it may also affect the HD brain. This is particularly relevant given the recent links between tau and HD disease progression.
“Noninvasive and low-cost circadian-based therapies such as light therapy may be promising for the management of sleep-wake disturbances in HD,” concludes Dr. Videnovic.
Reference :
- Sleep Disorders and Circadian Disruption in Huntington’s Disease – (https://content.iospress.com/articles/journal-of-huntingtons-disease/jhd230576)
Source: Eurekalert
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