<unk> is largely localized to the Fore people and people with whom they intermarried. The Fore people ritualistically cooked and consumed body parts of their family members following their death to incorporate "the body of the dead person into the bodies of living relatives, thus helping to free the spirit of the dead". Because the brain is the organ enriched in the infectious prion, women and children, who consumed brain, had a much higher likelihood of being infected than men, who preferentially consumed muscles. Normally folded prion protein PrPc subdomain-Residues 125–228. Note the presence of alpha helices (blue). Prion Cryoelectron Microscopy model of the misfolded PrPsc protein, enriched in beta sheets (center) The infectious agent is a misfolded form of a host-encoded protein called prion (PrP). Prion proteins are encoded by the Prion Protein Gene (PRNP). The two forms of prion are designated as PrPc, which is a normally folded protein, and PrPsc, a misfolded form which gives rise to the disease. The two forms do not differ in their amino acid sequence; however, the pathogenic PrPsc isoform differs from the normal PrPc form in its secondary and tertiary structure. The PrPsc isoform is more enriched in beta sheets, while the normal PrPc form is enriched in alpha helices. The differences in conformation allow PrPsc to aggregate and be extremely resistant to protein degradation by enzymes or by other chemical and physical means. The normal form, on the other hand, is susceptible to complete proteolysis and soluble in non-denaturing detergents. It has been suggested that pre-existing or acquired PrPsc can promote the conversion of PrPc into PrPsc, which goes on to convert other PrPc. This initiates a chain reaction that allows for its rapid propagation, resulting in the pathogenesis of prion diseases. Transmission In 1961, Australian medical researcher Michael Alpers conducted extensive field studies among the Fore accompanied by anthropologist Shirley Lindenbaum. 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. Alpers and Lindenbaum's research conclusively demonstrated that<unk> spread easily and rapidly in the Fore people due to their endocannibalistic funeral practices, in which relatives consumed the bodies of the dead to return the person's "life force" to the hamlet, a Fore societal subunit. Corpses of family members were often buried for days, then exhumed once the corpses were colonized by insect larvae, at which point the corpse would be dismembered and served with the larvae as a side dish. The demographic distribution evident in the infection rates –<unk> 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. Although ingestion of the prion particles can lead to the disease, a high degree of transmission occurred if the prion particles could reach the subcutaneous tissue. With elimination of cannibalism because of Australian colonial law enforcement and the local Christian missionaries' efforts, Alpers' research showed that<unk> was already declining among the Fore by the mid‑1960s. However, the mean incubation period of the disease is 14 years, and 7 cases were reported with latencies of 40 years or more for those who were most genetically resilient, continuing to appear for several more decades. Sources disagree on whether the last person with<unk> died in 2005 or 2009.
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