Research published in Nature by a team of British and Papua New Guinean scientists said the cannibalistic practice of eating a dead relative's brains has allowed one tribe in Papua New Guinea to develop a genetic resistance to a 'mad-cow like' disease.

This has proved to be useful for scientists who are studying diseases such as dementia. 

The people of the Fore tribe have been found to be resistant to a condition known as 'Kuru prion' which causes difficulty walking, swallowing and chewing.
It also causes loss of coordination and muscle twitching and becomes fatal within one year.

In a slightly ironic twist, while Kuru is actually caused by eating the infected brain of those with the disease, scientists believed that the continuation of the practice has resulted in the Fore tribe becoming immune to it, which has been dubbed as the "collective vaccine" effect.

The tribe members that survived were found to have the ‘prion resistance’ gene, which inhibits proteins from mutating and forming brain-damaging polymers.

Prions are infectious agents that cause fatal brain diseases such as CJD in humans, scrapie in sheep and BSE (bovine spongiform encephalopathy, or mad cow disease) in cattle.

Prions can also cause other conditions such as dementia, because the proteins change shape and stick together to form polymers that damage the brain. This also happens in other neurological diseases.

This could be part of the reason why survivors of the Fore tribe were also protected against disorders such as Parkinsons.

In the 1950s, the Kuru disease caused the death of up to two per cent of the population each year.

John Collinge of the Institute of Neurology’s prion unit at University College London, which co-led the work, said: "This is a striking example of Darwinian evolution in humans, the epidemic of prion disease selecting a single genetic change that provided complete protection against an invariably fatal dementia."

Mr Collinge added that his team would be conducting further research to understand the molecular basis of the disease.ADNFCR-2867-ID-801791193-ADNFCR

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