Sleep and circadian rhythm alterations correlate with depression and cognitive impairment in Huntington's disease

Exploring the Validity of the Short Version of the Problem Behaviours Assessment (PBA-s) for Huntington’s disease: A Rasch Analysis

“…across all levels of overall severity of behavioural symptoms, which is concordant with reports that the frequency of depression in women is higher in both HD and general populations [42][43][44]. Although significant DIF (i.e.…”

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

“…The morning rise phase of melatonin has also been shown to be delayed in HD individuals (19), which provides a mechanism underlying the delayed sleep-wake timing reported to occur in these patients (21,104). The precise mechanism responsible for the decrease or delayed melatonin levels observed in HD is unclear, but could potentially be attributed to the progressive neuronal dysfunction in the SCN (18,92).…”

“…Although the pathophysiology underlying the development and progression of these clinical features is complex, the accompanying alterations in neuroendocrine signalling, including cortisol (16,17) and melatonin (18,19) release, and changes in circadian rhythmicity (20,21) suggest that the activity of the hypothalamic-pituitary-adrenal (HPA) axis and the suprachiasmatic nucleus (SCN) are impaired in HD (see Table 1 for summary of HD pathologies relevant to this review). Neuropathological changes including volume loss, the loss of orexin-releasing neurons and decreased protein levels of vasoactive intestinal peptide (VIP) and arginine vasopressin (AVP) in the hypothalamus support this supposition (22)(23)(24).…”

Time-Restricted Feeding Improves Circadian Dysfunction as well as Motor Symptoms in the Q175 Mouse Model of Huntington’s Disease

“…Disturbances in the timing of sleep, typified by frequent bedtime awakenings, prolonged latency to fall asleep, and more naps during the awake phase, are extremely common in HD and often become apparent years before the onset of classic motor symptoms (Cuturic et al, 2009; Aziz et al, 2010a; Goodman et al, 2011). Similarly, mouse models of HD also exhibit a disrupted circadian rest/activity cycle that mimics the symptoms observed in human patients (Morton et al, 2005; Kudo et al, 2011; Loh et al, 2013).…”