The Laughing Death

I could tell you a story that features an exotic location, a plane crash, an isolated cannibalistic tribe, gold-diggers, a bizarre disease, experiments on chimpanzees, tribal wars, the transmission of brain proteins like infectious agents, allegations of child abuse, mad cows, imprisonment of the main character, his exile within the Arctic circle, as well as the two Nobel Prizes in medicine. You could then say: “Sure, anyone can just make anything up”. And that’s fair enough, but… what if this was a true story?

The Fore tribe lives in the Okapa area of the Eastern Highlands of Papua New Guinea. Their habitat is formed by about a thousand square kilometres of pristine forest, with the rainy season occurring between December and March. Their population size may be reaching about twenty thousand and their people are separated by the Wanevinti Mountains in the northern and southern regions. They survive thanks to farming, they’re polytheist, and they use three different dialects of their language. The Fore tribe intrigued the international public between 1957 and 1960, as they recorded about 1,000 deaths from a new and unknown disease — Kuru disease, named after their word ‘’kuria’’, which meant “shake/tremble.” The disorder has also become known as “the laughing sickness”, due to the pathological attacks of laughter that accompany the condition.

Up until the 1950s, the Fore tribe managed to avoid any contact with the rest of the world. It was noted only that one plane had crashed into the area in which they lived during World War II. With the establishment of the Okapa police station in 1951, by order of the Australian authorities, law enforcement officials visited the villages of the Fore tribe, explaining to them the importance of hygiene and road construction. They also sought to dissuade them from three traditional tribal practices — constant warfare between villages, witchcraft and cannibalism. The officials explained their economics and trade, based on money, and taught them the so-called “pidgin” variants of the English language. The younger members of the Fore tribe embraced these innovations more readily than the older members, especially as it gave them an excuse to stop participating in the constant battles between the villages, into which the older leaders have often pushed them.

The Fore tribe believes in the existence of five souls, each of which should end up in the correct place following death. Based on this belief system, they conduct cannibalistic rituals, eating their dead to ensure that the tribe would preserve all of the important talents and other positive aspects of the deceased. They believe that all those positive aspects are contained in two souls, while the remaining three souls are to travel to “kwelanandamundi”, the land of the dead. The sorcerers within the village, who controlled the aforementioned cannibalistic rituals, were originally thought of as defenders of the village. However, the epidemic of Kuru disease caused a change in attitude towards the sorcerers. Suddenly, it seemed to the villagers that their spells could be causing the illness. This led to community meetings of all village members. They were trying to make an appeal to these “unknown sorcerers” among the population, asking them publicly to stop casting their spells because it was increasingly obvious that they “didn’t know what they were doing”. Meanwhile, patrol officers from the outside world believed that Kuru disease was a psychosomatic or mental illness, triggered by the trauma caused by Western colonisation. In 1951, Arthur Carey first used the term Kuru in his report to describe a new disease that had struck the tribe, noting that Kuru disease mainly affects women and eventually kills them. After Carey, police officer John McArthur described the disease in his report in 1953.

A mix of several significant causes, such as Australian hegemony in the region, centralised governance, the establishment of courts, increasing investment and trade development, and the pre-existing desire of the youth in the Fore tribe to end the warfare, have all combined to eventually secure lasting peace in the region. Foreign influences brought about a significant change in the culture of the Fore tribe, influencing them both directly and in an indirect sense. From the 1950s to the 1970s, foreign presence in the Fore region was increasingly pronounced. In addition to Australian colonial forces, scholars studying local diseases and Christian missionaries visited the region. The original polytheistic religion was slowly replaced by Christianity. And that change is partly responsible for the abandoning of the ritual of consuming deceased relatives, which was the most likely cause of the spread of the Kuru disease epidemic. The frequent presence of scientists and medical experts interested in researching Kuru disease resulted in the expansion of foreign infrastructure, technology and cultural practices in the area. These processes were faster than could have been expected, accelerating cultural change.

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Kuru disease is a rare and incurable disorder, the main feature of which is the degeneration of nerve cells, i.e. neurons. But its feature that really captivated the interest of the scientific community was that the disease seemed to be transmissible. This was unexpected, because the degeneration of anything within the body, and especially neurons, was considered a consequence of the “wear and tear of material” over time. Therefore, degenerative diseases were considered to be non-communicable, “private” human diseases. They would develop within us owing to specific individual causes, and at their own pace. That is why scientists were so surprised that a disease in which neurons clearly fail, leading to a loss of coordination, loss of control over muscle movement, uncontrollable outbursts of laughter, and finally death, could in any way be transmitted from person to person — even if the practice of cannibalism had anything to do with transmissibility.

Kuru disease was indeed very interesting, because of a range of its characteristics. The symptoms didn’t begin immediately after the infection, but quite the opposite. This silent phase, called “the incubation period”, would last — on average — between ten and fifteen years. The fastest development of symptoms was described to have occurred after five years, and the longest delayed infection by as much as fifty years. Therefore, the youngest person with severe symptoms was an 11-year-old child. Such a long incubation period is extremely unusual for any infectious disease and has indicated the possibility of a long period between infection and the onset of symptoms in at least some infectious diseases.

When symptoms finally do appear, the disease usually lasts for about a year. In the first phase of the disease, also called “the walking phase”, the affected person begins to show instability in standing and walking, decreased control of their muscles that start to tremble, and difficulty in saying some words. In the second phase, called “the sedentary phase”, walking is no longer possible without support. Also, there are more tremors, coupled with emotional instability and depression, with occasional outbursts of uncontrollable laughter. In the final stages, the diseased person can no longer sit without someone else’s support and finds it increasingly difficult to swallow, which is why they lose weight very quickly. They can no longer willingly control their bladder or bowel movements. Eventually, they entirely lose their ability to speak and they stop responding to environmental stimuli. Their death occurs from pneumonia or a generalised infection arising from the ulcers that begin to form on their skin.

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The first foreigners to notice the symptoms of Kuru disease among the Fore tribe were European gold-seekers back in the 1930s and 1940s. The disease was first documented by anthropologists Ronald Berndt and Catherine Berndt in 1953. However, anthropologists Shirley Lindenbaum and Robert Glasse were the first to formally publish the hypothesis that Kuru disease may be spreading because of cannibalism. The anthropologist who dedicated himself to the disease, Daniel Carleton Gajdusek, also suspected that to be the case. This possibility intrigued them all because adult women, as well as children of both sexes, were affected eight times more often than adult men were. Such age and gender distribution of the disease made no sense, nor did it coincide with any other known disease. Anthropologists Lindenbaum and Glasse, as well as Gajdusek, realised that in the cannibalistic rite, women and children most commonly consume the brain of the deceased, while adult men consume muscle, to give them strength. Women consumed the internal organs because the soul, called “kwela”, was considered dangerous if it was not properly taken care of, and the female womb was supposed to be the safest place to dispose of it.

When a member of the Fore tribe died, mourning lasted for two to three days. Then, the women would cut up and cook the body and prepare it for consumption, an act in which the men would very rarely participate. They made sure, according to their teachings, to consume all of the body parts carefully, including even drying, crushing and consuming the bones mixed with vegetables, so that nothing was left behind. The series of purification rituals, which were supposed to purify the “kwela”, would take several weeks, sending all of the remaining parts of the soul into the land of the dead during the rites.

The prevalence of Kuru disease among the Fore tribe increased significantly in the 1940s and 1950s. The death rate began to approach the figure of as many as four deaths per hundred inhabitants per year, occurring in a population that then only amounted to about 12,000 people. It was particularly worrying to the Fore tribe that mainly their women and children were affected. Therefore, the numerical relationship between women and men became distorted over the two decades, reaching a ratio of one woman to two men. Over time, this had worsened to even one woman to three men in the southern regions. Because of the deaths of their women of fertile age and their children, Kuru disease began threatening the Fore people with extinction in the late 1950s. Following the outbreak of Kuru disease, the Australian Government banned the cannibalistic rite and strictly controlled the tribe, aiming to interrupt the transmission of Kuru disease. Still, cannibalism had been practised for longer in the southern part of the tribe than it had been in the north. Once the cannibalism was abandoned, the incredibly long “quiet” incubation period meant that infected people still continued to appear for decades — though, thankfully, less frequently. Sources don’t fully agree on whether the last patient died in 2005 or 2009, but there have been no new cases since.

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This rare and unusual disease was eventually understood in several steps. The research related to the laughing sickness eventually led to the discovery of entirely new mechanisms of infection between humans. It also resulted in two different Nobel Prizes in Medicine, those awarded in 1976 and 1997. To understand and appreciate how this was achieved, we need to return back to 1920, when the so-called Creutzfeldt-Jakob disease (CJD) was first described.

Creutzfeldt-Jakob disease is a universally deadly brain disease. It is incredibly rare and it affects only one in a million people each year. Early symptoms include memory problems, behavioural changes, poor coordination, and visual disturbances. Later on, memory loss increases. Unconscious movements, blindness, weakness and coma appear. About 90 per cent of patients, most often in their 60s, will die within a year of diagnosis. The German neurologist Hans Gerhard Creutzfeldt first described a similar disease in 1920. Shortly afterwards, in 1921, another German scientist, Alfons Maria Jakob, described several cases independently of Creutzfeldt in three scientific papers. As Jakob thought that Creutzfeldt has already described the first such case, he fairly called the disease Creutzfeldt-Jakob disease.

But Creutzfeldt later said, also fairly, that the case he had described had nothing to do with what Jakob managed to observe and describe. So, this rare disease should actually be called Jakob’s disease and Jakob had unnecessarily put himself in second place. However, in scientific literature, this disease has quickly become so commonly known as Creutzfeldt-Jakob’s disease that Creutzfeld, neither guilty nor obliged, became recognised among all physicians across the world and became a well-known part of the history of medicine. To achieve this, he described only one case of brain disease that was not Creutzfeldt-Jakob disease, but Jakob then glorified him by his misconception. Regardless, there were no scientists at the time who had any clue why this disease was occurring.

While German scientists were raising awareness of a strange brain disease, something very unusual was happening in the same time period in a completely different part of the world. One of the older members of the Fore tribe in Papua New Guinea was affected by Creutzfeldt-Jakob disease. This is not unexpected in itself, because the disease affects one in a million people, so it can potentially occur anywhere and affect anyone. But in the Fore tribe, as we already know, deceased members of the tribe were cooked and then consumed, to “free their souls”. Tribal men ate muscle and women and children ate brains. So, whatever caused Creutzfeld-Jakob disease in the human brain, if it was contagious, this rare case gave it a truly unexpected opportunity to spread to other people, who wouldn’t otherwise be affected by the disease. Indeed, after a long period of dormancy — of ten to fifteen years -the epidemic of Kuru disease erupted in the Fore tribe in the 1940s and 1950s.

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Several anthropologists became intensely interested in studying this disease. Daniel Carleton Gajdusek, born in the state of New York, was certainly one of them. He graduated from the University of Rochester during World War II and studied physics, biology, chemistry and mathematics there. He then completed his medical studies at Harvard University and began his postgraduate research at Columbia Universities in New York, the California Institute of Technology and Harvard. During his military service, he was assigned as a virus specialist at the Walter Reed Military Medical School. After serving in the Army, in 1954 he joined as a researcher at the Walter and Eliza Hall Institute in Melbourne, Australia. From that location, he could begin his devoted work to investigate the then-already-present Kuru disease epidemic among the Fore tribe.

He was introduced to the Kuru problem by Vincent Zigas, the district medical officer in charge of Papua New Guinea. Gajdusek lived among the tribe, studying their language and culture, and performing autopsies on the victims of Kuru disease. He presented the first detailed medical description of the disease, for which the name “the laughing sickness” soon became popular with the press. He also linked the spread of the disease to the practice of ritualistic cannibalism and decided to prove that neurodegenerative disease can be transmitted as infectious. He wasn’t able to ethically study humans, so he needed a species as similar to humans as possible. He opted for chimpanzees. He would drill holes in the skulls of sedated chimpanzees and inject the purified brain matter of a girl who had died from Kuru disease into the brain of the chimpanzee. A sample of this young Kuru patient’s tissue was supplied to him by Australian physician Michael Alpers, who was conducting field research among the Fore tribe at the time. Then, Gajdusek had to continue feeding the chimpanzees and wait for several years. It was risky research because he needed to hope that the chimpanzees would not die and that they would indeed develop the disease. There were no guarantees for either of these two outcomes because no one knew if there was an infectious agent involved. An additional problem was that even if there was, it may have only been dangerous to humans, while it could not affect chimpanzees.

Researcher Joe Gibbs joined Gajdusek and fully accepted the risk of failure. He was monitoring and recording the behaviour of the monkeys and conducted their autopsies. Given all of the uncertainties surrounding this bold experiment, it is truly remarkable that it eventually succeeded. Within two years, one of the chimpanzees, Daisy, developed symptoms of Kuru disease. This proved that an unknown infectious disease agent was being transmitted through biological material. Clearly, it was capable of infecting other primates, not just humans. Importantly, Elisabeth Beck soon confirmed the result of this experiment with her team, which truly strengthened the conclusion. This was the first demonstration in the history of medicine that degenerative human disease can spread like an infectious disease.

However, during all those years of waiting for chimpanzees in Gajdusek’s laboratory to become unwell, research into Kuru disease had been rife with controversy and conflicts of opinion among researchers who had addressed the issue. For example, anthropologist Willam Arens criticised reports of cannibalism in the Fore tribe and claimed that Gajdusek couldn’t have witnessed cannibalism, as researchers working with the Fore tribe in the 1950s allegedly claimed that cannibalism had been dismissed in 1948. This was while Gajdusek was still in the United States, years before he moved to Australia. Arens also argued that the stories of cannibalism were exaggerated and often contradictory, that the incidence of Kuru disease had declined since the arrival of the Europeans in the area, and their impact on the development of the Fore tribal settlements and the improvements in their living conditions — with the introduction of schools and health care — was a more likely explanation for the disappearance of the disease.

Contrary to Arens’s criticism, other anthropologists, including R. Klitzman, S. Lindenbaum, and R. Glasse, as well as local researchers from Papua New Guinea, clearly documented the practice of cannibalism among members of the Fore tribe. Australian researcher Michael Alpers conducted extensive field research on the Fore tribe, accompanied by anthropologist Shirley Lindenbaum in the early 1960s. They concluded that the epidemic of Kuru disease could have started as early as 1900, beginning with only one person.

This person, as mentioned above, spontaneously developed some form of Creutzfeldt-Jakob disease, which then continued to be transmitted to the women and children of the Fore tribe through cannibalism. A possible route of transmission was the cleaning up of deceased relatives after death, because of contact with any open sores or wounds on the hands. That was considered sufficient for the infectious agent in the subcutaneous tissue to cause infection.

With all this taken into account, the successful experiment on the chimpanzees was received as truly spectacular, considered very solid, and was accepted by the biomedical research community. In 1958, Gajdusek was appointed head of the Virological and Neurological Research Laboratory at the American National Institutes of Health — the NIH. Sixteen years later, in 1974, he became a Fellow of the American National Academy of Sciences, in the discipline of microbial biology. Two years later, in 1976, he was awarded the Nobel Prize in Physiology or Medicine, which he shared with Baruch S. Blumberg, a pioneer in research into the hepatitis B virus.

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It has now become clear that something, which resided in the tissue of the diseased brain, could also enter other people’s body and lead to the same symptoms. But what could it be? Bacterium? A virus? A parasite? E. J. Field took over the conduct of research in Papua New Guinea in the late 1960s and early 1970s, exploring the disease further. Kuru disease seemed to have similarities with the so-called “scrapie” in sheep and goats. That is also an unusual and insufficiently explained neurodegenerative disease. He noticed that the so-called glial cells played a role. Significantly, he also observed that the process of infection, whatever its cause, may in some way depend on the change in the structure of the affected person’s molecule. This insight was an early precursor to an entirely new system of ideas in biology, which would later become known as the “prion hypothesis.” Along with its resemblance to “scrapie”, evidence was also gradually mounting that Kuru disease shared many properties with Creutzfeldt-Jakob disease. Gajdusek himself stated that it was most likely that an entirely new pathogen, which was unknown to science, was at the root of Kuru disease, Creutzfeldt-Jakob disease and “scrapie”.

Important molecular studies of the aforementioned diseases involved Stanley Benjamin Prusiner, an American neurologist and biochemist. Today, he is the director of the Institute of Neurodegenerative Diseases at the University of California, San Francisco (UCSF). However, in the early 1970s, Prusiner investigated the so-called “spongiform encephalopathies”. These were degenerative changes in the brain, such as those with Kuru disease, where the brain gradually becomes like a sponge, i.e. “spongiform”, due to numerous small changes caused by nerve tissue degeneration. Prusiner worked specifically on the beef subspecies, the so-called “mad cow disease”. He realised that he could explain both “mad cow disease” and Creutzfeld-Jakob disease, which are actually both very close in class to infectious, self-reproducing proteins.

Therefore, it should be understood that among infectious agents parasites are real, multicellular small organisms. Unlike them, bacteria only have one cell, while viruses have only an RNA or DNA molecule with a protein envelope. However, these peculiar proteins, which seemed to be able to multiply, formed a whole new category of infectious agents. In his 1982 work, Prusiner called them “prions”. He came to this name by linking the words “protein” and “infection” to indicate that this is a previously unknown form of an infectious pathogen, built solely from protein.

These “spongiform encephalopathies”, which are indeed contagious in their nature — although they may be better off being called “transmissible” because they don’t tend to spread from organism to organism like most other infectious agents do — are probably caused by prions. Prions are proteins that are otherwise expected to occur in healthy central nervous system neurons. These proteins, however, when misfolded, are likely to damage signalling processes, damage neurons and result in their degeneration, which over time also leads to the characteristic sponge-like appearance of the afflicted brain. Infectious prions are misfolded proteins that can prevent correctly folded proteins from proper dissolution and function. Most cases of prion diseases occur spontaneously for no apparent reason, while just under a dozen cases are inherited from parents by autosomal dominant inheritance. Infection can occur owing to exposure to the brain tissue or nerve tissue of the spinal cord of an infected person.

The prion found in Creutzfeldt-Jakob disease is dangerous because it stimulates normal variants of the protein to rewind to a state which is misfolded and dysfunctional. In doing so, the number of misfolded proteins begins to increase exponentially, leading to the accumulation of vast amounts of insoluble proteins in the affected brain cells. This mass of dysfunctional proteins interferes with the function of neuronal cells and causes their death because cell cleansing mechanisms cannot digest misfolded proteins. When a prion is transferred to another person, these dysfunctional proteins move into the brain and induce the normal prion protein molecules there to misfold. That is why all neurodegenerative diseases of this type are commonly referred to as “prion diseases”.

As further proof of the prion hypothesis, humans can develop Creutzfeld-Jakob disease by possessing a mutation in the gene that encodes prion protein (PRNP). This mutation is only found in every tenth to the twentieth case of the disease. It is not clear why the disorder occurs in all other cases. Less than 1 per cent of patients have a so-called “variant of Creutzfeldt-Jakob disease” (vCJD). It is a different disease that can potentially be acquired through the infection of humans with bovine spongiform encephalopathy, i.e., “mad cow disease”. This extremely rare subtype of Creutzfeldt-Jakob disease can be caused by eating foods contaminated with prions, such as beef burgers. The basic feature of this CJD variant is that it affects people of a much younger age, such as those in their 20s.

Thanks to his “prion hypothesis”, which combined several truly mysterious diseases into the same group and suggested a common cause, Stanley B. Prusiner was awarded the Lasker Prize in 1994 and then the 1997 Nobel Prize in Physiology and Medicine, „for his discovery of Prions — a new biological principle of infection”.

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The scientific breakthrough in genetics and molecular medicine in the 21st century has made it possible to analyse the genes and proteins of members of the Fore tribe to investigate whether there may be individuals in the tribe who are somehow “protected” from the disease. Scientists at University College London have identified a genetic mutation that provides members of the tribe with protection against prion diseases. They achieved this by finding a naturally occurring version of the prion protein, which makes resistance to Kuru disease possible. They surveyed more than 3,000 people from the Fore tribe and showed that there was a mutation, the so-called “G127 polymorphism”, which leads to the synthesis of a prion protein associated with strong resistance to Kuru disease. Further evidence in support of this finding is that the mutation is widespread in an area where Kuru disease endangered people’s lives, while it is extremely rare elsewhere in the world. It can also be estimated that among the Kuru tribe, this mutation has been under positive selection for the past 10 generations, which is consistent with the knowledge about the role of Kuru disease in endangering the tribe. This is an extremely clear example of the process of Darwin’s natural selection in a human population, as this mutation represents a population response to a truly threatening disease. Such a result might help us to understand how we can protect ourselves against prion diseases, and the knowledge of natural resilience might be used to combat Creutzfeldt-Jakob disease as well as Alzheimer’s disease. Some scientists also believe that the fact that this mutation is not widespread among other populations in the world may mean that cannibalism and dying from prion diseases have probably not been widespread throughout human history.

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For decades, the Kuru disease story has interested not only the biomedical scientific community but the entire international public. Fascination with an exotic location, a tribe that comes into contact with civilisation, cannibalism as a way of spreading the contagion, transmitting the personal degenerative disease to other people like an infection, a silent period of disease spanning many decades, and new and completely unknown carriers of the disease — prions, as well as the two Nobel Prizes awarded for the work undertaken on the disease have helped to keep the public interested in any new piece of news or publication related to this story. So, that’s how this story got two more unexpected sequels, which drew considerable media attention.

During his research trips to Papua New Guinea, Nobel laureate Daniel Carleton Gajdusek brought as many as 56, mostly male children, back to the US to live with him. There, he gave everyone the opportunity to finish high school and get a college education. One of those children, in adulthood, accused Gajdusek of abusing him as a child, and in 1996 Gajdusek was indeed charged with child abuse, based on some incriminating records found in his personal diary, as well as statements made by the victim. The case caused a lot of controversies as there were also opinions that Gajdusek’s entire case could have been framed on him owing to various, insufficiently transparent, struggles for power within this very promising new area of research. Edinburgh-based psychologist Chris Brand was particularly vehement in attacking the process against Gajdusek, calling it overly strict and anti-elitist.

According to official reports, Gajdusek pleaded guilty in 1997 and was sentenced to 12 months in prison and served his sentence in the United States. Following his release from prison in 1998, he was also given five years of further supervision, to which he was to be subject to a court order, but was allowed to serve those years in Europe. Gajdusek left the US and went on a self-declared exile to Amsterdam, never returning to the US again. He then lived in Paris, and at the end of his life, he lived in Tromsø, Norway. This place has 24 hours of darkness in the winter, and the isolation and darkness helped him to concentrate on his work even during those later years. He died there at the end of 2008, at the age of 85, having actively worked for the rest of his life.

Following his death, the 2009 documentary by Bosse Lindquist called “The Genius and the Boys” premiered on the BBC. The documentary explored the background of this court process and revealed that the seven boys Gajdusek brought with him to the US testified in complete secrecy about how Gajdusek involved them in sexual activities while they were boys. Four did not claim the experience to have been traumatic, but the remaining three did. Throughout the film, he sought to penetrate the various elements of this controversy, identify motives on both sides, and better understand Gajdusek’s views on life, research, human sexuality, as well as his motives for bringing so many boys to the United States, as well as his complete lifelong commitment to science. Inspired by this unusual life story, Hanya Yanagihara published the 2013 novel “The People in the Trees.” In this novel, the life story of the main character, A. Norton Perin is clearly inspired by Gajdusek’s life.

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This whole strange story related to Kuru disease is still wrapped in a dose of uncertainty in everything that we know about it today, and surprises are still possible. During the 21st century, the number of extremely old people increased and the incidence of a specific type of memory loss known as Alzheimer’s disease began to increase. Two important features of this disease are the build-up of a peptide called amyloid-beta, as well as plexus of the so-called tau-protein. It could be concluded that this is also a prion protein, and another new and very important prion disease. However, it isn’t clear enough whether, in Alzheimer’s disease, the accumulation of these proteins is the primary process leading to the disease, or just the consequence of another disorder that has another cause. This has led to a re-assessment of prion diseases, as some researchers have begun to question whether, based on the mere presence of prion proteins in the brain, it is still too quickly concluded and accepted that they are the primary cause of the disease, and not perhaps the consequence of some other mechanism.

Back in early 2007, a neuropathologist at Yale University, Laura Manuelidis, questioned the explanation for Kuru disease being caused by a prion protein disorder. She reported that her team had found a viral particle that could be the primary driver of the pathological processes associated with Kuru disease. We now need to wait for new evidence and confirmations from other researchers, and after a long time, we need to look at them in the light of the latest research advances. Only then should we infer what the most likely explanation for the Kuru disease and other very rare, but extremely deadly, so-called “prion diseases” might be.

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Declaration: Professor Igor Rudan, FRSE, is the President of the International Society of Global Health; co-Editor-in-Chief of the “Journal of Global Health”; Joint Director of the Centre for Global Health and the WHO Collaborating Centre at the University of Edinburgh, UK.

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Image credit: Screenshot from a documentary series on Kuru disease.