Every animal that’s been studied intensively does have periods of reduced activity and reduced responsiveness, and does get extra ‘rebound’ sleep after a period of researcher-induced sleep deprivation. Yet Cirelli & Tononi 2008 argue that in fact there is no convincing example of an animal that doesn’t sleep. Or at least, an animal that doesn’t need extra recovery sleep following sleep deprivation, or an animal for whom sleep deprivation does not have serious consequences. They toy with this idea and then propose that if the null hypothesis is actually true – sleep has no core essential function across species – then we should be able to find at least one animal that never sleeps. Therefore Cirelli & Tononi 2008 open by challenging the idea that sleep is essential, proposing that perhaps the reason we haven’t found its core function yet is because it has none. If so, scientists still don’t know what that role is. If we believe that all animals sleep, despite the high cost to doing so, then there must be some really fundamental biological role that sleep plays which is conserved across all animal species. As Sehgal & Mignot 2011 put it:Īs a state that seemingly freezes all productive activity and puts animals in danger of being caught by predators, sleep must serve an important purpose because it has survived many years of evolution.

Many scientists have assumed, for decades, that all animals sleep by this definition. To get at a broader swath of the animal kingdom, researchers now define sleep in terms of (as described above) reduced activity and reduced responsiveness to stimulation. For other species it is somewhat more logistically difficult to record electrical activity in the brain, though incredibly, people have done it, even in fruit flies. Researchers have quantified these features in other mammals and birds as well and they seem to at least partially fit the human conception of sleep in terms of brain activity. Sleep quantity and quality are often measured in EEG terms if you ever participate in a sleep study they’ll probably measure your brain activity with an EEG in addition to your heart rate, eye movements, blood pressure and other things. Spindles are characteristic of Stage 2 sleep each stage of sleep in humans has its own characteristic EEG appearance as well as behavioral features. They are clearer on this Wikipedia graphic: The loss of them is characteristic of fatal familial insomnia. “ Spindles” are the really dense, short waves seen in stage N2 above. In humans, sleep is usually characterized based on EEG waveforms ( Cirelli 2009 Fig 1b): This definition is intentionally general to allow it to encompass species very different from us. The decreased ability to react to stimuli distinguishes sleep from quiet wakefulness, while its reversibility distinguishes sleep from coma. Sleep is a reversible condition of reduced responsiveness usually associated with immobility. And Landholt 2006 has also noted sleep phenotypes in familial CJD.Īs I got deeper into Cirelli 2009, I realized I needed to start from a more basic first step: what is sleep, physiologically and molecularly speaking? Cirelli & Tononi 2008, in an article provocatively entitled “Is Sleep Essential?”, define sleep as follows: Tobler 1996 and Tobler 1997 ( ft) showed that PrP knockout mice have subtly altered circadian rhythms and sleep EEGs, a point I’ll return to later in more detail. And PrP’s connection to sleep is not just through FFI either. (Fatal familial insomnia had already been characterized – and named – by Lugaresi 1986, but the causal gene wasn’t yet known then). When Medori 1992 ( ft) linked FFI to the D178N mutation, PRNP became the first gene known to be involved in sleep. I started with a review by Cirelli 2009 and was surprised to learn, in the second sentence, that FFI is considered a big deal in sleep science. I have never been clear on why FFI affects sleep: is it just because it kills neurons in the thalamus, where sleep/wake is regulated? Or do FFI prions directly interfere in sleep pathways? So I decided to dig up some reviews on sleep science and see what the world knows about sleep at the molecular level. It is being left online for historical reasons, but read at your own risk.įatal familial insomnia is a prion disease, more broadly a protein-folding disease and a neurodegenerative disease, and those are the angles from which it is most often studied. The original author no longer endorses the content of this post. This post was written during early stages of trying to understand a complex scientific problem, and we didn't get everything right. Fatal familial insomnia as a sleep disorder

Fatal insomnia