[5] While the Fore people stopped consuming human meat in the early 1960s, when it was first speculated to be transmitted via endocannibalism, the disease lingered due to kuru's long incubation period of anywhere from 10 to over 50 years.

[7][8][9][10] Kuru, a transmissible spongiform encephalopathy, is a disease of the nervous system that causes physiological and neurological effects which ultimately lead to death.

[14] In the ambulant stage, the infected individual may exhibit unsteady stance and gait, decreased muscle control, difficulty pronouncing words (dysarthria), and tremors (titubation).

[14] In the terminal stage, the infected individual's existing symptoms, like ataxia, progress to the point where it is no longer possible to sit up without support.

New symptoms also emerge: the individual develops dysphagia, which can lead to severe malnutrition, and may also become incontinent, lose the ability or will to speak, and become unresponsive to their surroundings despite maintaining consciousness.

These studies by Klatzo et al., found that neurons in a Kuru infected brain were abnormally small and lighter in color compared to their healthy counterparts.

[20] The differences in conformation allow PrPsc to aggregate and be extremely resistant to protein degradation by enzymes or by other chemical and physical means.

[14] In 1961, Australian medical researcher Michael Alpers conducted extensive field studies among the Fore accompanied by anthropologist Shirley Lindenbaum.

[9] Their historical research suggested the epidemic may have originated around 1900 from a single individual who lived on the edge of Fore territory and who is thought to have spontaneously developed some form of Creutzfeldt–Jakob disease.

[25] The demographic distribution evident in the infection rates – kuru was eight to nine times more prevalent in women and children than in men at its peak – is because Fore men considered consuming human flesh to weaken them in times of conflict or battle, while the women and children were more likely to eat the bodies of the deceased, including the brain, where the prion particles were particularly concentrated.

Also, the strong possibility exists that it was passed on to women and children more easily because they took on the task of cleaning relatives after death and might have had open sores and cuts on their hands.

With elimination of cannibalism because of Australian colonial law enforcement and the local Christian missionaries' efforts, Alpers' research showed that kuru was already declining among the Fore by the mid‑1960s.

[27][28] There is no laboratory test to determine the presence of Kuru, except for postmortem evaluation of central nervous system (CNS) tissues, so diagnoses are achieved by eliminating other possible disorders.

[29] Periodic complexes (PC), reoccurring patterns with spike wave-complexes occurring at intervals, are recorded frequently in some diseases but are not presented in the kuru readings.

In the study, which began in 1996,[31] researchers assessed over 3,000 people from the affected and surrounding Eastern Highland populations, and identified a variation in the prion protein G127.

[7] Michael Alpers, an Australian doctor, collaborated with Gajdusek by providing samples of brain tissues he had taken from an 11-year-old Fore girl who had died of kuru.

Within two years, one of the chimps, Daisy, had developed kuru, demonstrating that an unknown disease factor was transmitted through infected biomaterial and that it was capable of crossing the species barrier to other primates.

Field spent large parts of the late 1960s and early 1970s in New Guinea investigating the disease,[42] connecting it to scrapie and multiple sclerosis.

[43] He noted the disease's interactions with glial cells, including the critical observation that the infectious process may depend on the structural rearrangement of the host's molecules.