The Role of the Mammalian Prion Protein in the Control of Sleep

Roguski, Amber; Gill, Andrew C.

doi:10.3390/pathogens6040058

Cited by 10 publications

(7 citation statements)

References 80 publications

(107 reference statements)

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“…In our analysis, the top predicted target of differential miRNAs was PrP C , a cell surface protein mainly known for its notorious role in prion diseases (Wulf, Senatore, & Aguzzi, ). Of note, recent evidence suggests a role of PrPC in sleep regulation through noradrenergic and dopaminergic signalling and melatonin synthesis, possibly modulating both healthy circadian activity rhythms and patterns, and sleep dysfunction during neurodegenerative disorders (Roguski & Gill, ).…”

Section: Discussionmentioning

confidence: 99%

Circulating miRNAs are associated with sleep duration in children/adolescents: Results of the I.Family Study

Iacomino

Lauria

Russo

et al. 2020

Experimental Physiology

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It is commonly recognized that sleep is essential for children's health, and that insufficient sleep duration is associated with negative health outcomes. In humans, sleep duration and quality are influenced by genetic, environmental and social factors. Epigenetic mechanisms, likewise, regulate circadian rhythms and sleep patterns. In the present study, we aimed to identify circulating microRNAs associated with sleep duration in a subsample of normal-weight European children/adolescents (n = 111) participating in the I.Family Study. Subjects were divided into two groups based upon self-reported sleep duration, according to the recommended amount of sleep for paediatric populations. Sleep needs for children <13 years were at least 9 h per day, and for children >13 were at least 8 h per day. There were group differences (short sleepers versus normal sleepers) in circulating levels of miR-26b-3p (mean (95% CI) = 2.0 (1.3-2.7) versus 2.3 (1.9-2.7), P = 0.05) and miR-485-5p (mean (95% CI) = 0.6 (0.3-0.9) versus 0.9 (0.7 -1.0), P < 0.001), adjusting for country of origin, age, sex, pubertal status, screen time and highest educational level of parents. Our findings show for the first time that sleep duration reflects the profile of specific circulating microRNAs in school-aged children and adolescents. It is conceivable that epigenetic modifications, mainly related to circadian rhythm control, may be modulated or interfere with sleep duration.

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Section: Discussionmentioning

confidence: 99%

Circulating miRNAs are associated with sleep duration in children/adolescents: Results of the I.Family Study

Iacomino

Lauria

Russo

et al. 2020

Experimental Physiology

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“…In conclusion, the use of PLR mediated by mRGCs, as a measure of mRGC function, is of particular relevance for neurodegenerative disorders for which there is already evidence of circadian and sleep dysfunction, such as PD, AD, and HD. Similarly, it might be also relevant for other neurological disorders with evidence of circadian dysfunction such as frontotemporal dementia (71), Lewy-Body dementia (72), Progressive Supranuclear Palsy (73, 74), and possibly prion diseases, in particular fatal familial insomnia (75). Moreover, the study of PLR mediated by mRGCs might be particularly intriguing for conditions, in which light sensitivity is a predominant feature, such as photophobia (76, 77) and photosensitivity in epilepsy (78).…”

Section: Discussionmentioning

confidence: 99%

Melanopsin Retinal Ganglion Cells and Pupil: Clinical Implications for Neuro-Ophthalmology

2018

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Melanopsin retinal ganglion cells (mRGCs) are intrinsically photosensitive RGCs that mediate many relevant non-image forming functions of the eye, including the pupillary light reflex, through the projections to the olivary pretectal nucleus. In particular, the post-illumination pupil response (PIPR), as evaluated by chromatic pupillometry, can be used as a reliable marker of mRGC function in vivo. In the last years, pupillometry has become a promising tool to assess mRGC dysfunction in various neurological and neuro-ophthalmological conditions. In this review we will present the most relevant findings of pupillometric studies in glaucoma, hereditary optic neuropathies, ischemic optic neuropathies, idiopathic intracranial hypertension, multiple sclerosis, Parkinson's disease, and mood disorders. The use of PIPR as a marker for mRGC function is also proposed for other neurodegenerative disorders in which circadian dysfunction is documented.

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“…There has been a longstanding interest in the role of PRPC in sleep particularly as mutations in PRPC cause the prion disease fatal insomnia. PRPC regulates sleep and circadian rhythmicity (Roguski and Gill, 2017) and mouse studies indicate roles in governing sleep cycles and regulating sleep after periods of sleep deprivation (Dossena et al, 2008;Tobler et al, 1997).…”

Section: Norepinephrine Modulation Of Learning and Aβ Depositionmentioning

confidence: 99%

Alzheimer’s disease as a syndrome of overloaded amyloidic synaptic tagging in memory networks

Murphy¹

2021

Preprint

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Alzheimer’s Disease is defined as progressive memory loss coincident with accumulation of aggregated amyloid beta and phosphorylated tau. Identifying the relationship between these features has guided Alzheimer’s Disease research for decades, principally with the view that aggregated proteins drive a neurodegenerative process. Here I propose that amyloid beta and phospho-tau write-protect and tag neuroplastic changes as they form, protecting and insuring established neuroplasticity from corruption. In way of illustration, binding of oligomeric amyloid beta to the prion receptor is presented as an example possible mechanism. The write-protecting process is conjected to occur at least partially under the governance of isodendritic neuromodulators such as norepinephrine and acetylcholine. Coincident with aging, animals are exposed to accumulating amounts of memorable information. Compounded with recent increases in life expectancy and exposure to information-rich environments this causes aggregating proteins to reach unforeseen toxic levels as mnemonic circuits overload. As the brain cannot purposefully delete memories nor protect against overaccumulation of aggregating proteins, the result is catastrophic breakdown on cellular and network levels causing memory loss.

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The Role of the Mammalian Prion Protein in the Control of Sleep

Cited by 10 publications

References 80 publications

Circulating miRNAs are associated with sleep duration in children/adolescents: Results of the I.Family Study

Circulating miRNAs are associated with sleep duration in children/adolescents: Results of the I.Family Study

Melanopsin Retinal Ganglion Cells and Pupil: Clinical Implications for Neuro-Ophthalmology

Alzheimer’s disease as a syndrome of overloaded amyloidic synaptic tagging in memory networks

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