The DNA of tribes in a remote location of Papua New Guinea may perhaps someday assist scientists discover a way to shield persons from certain degenerative brain illnesses, including the illness generally called “mad cow” disease.
Even though studying the Fore population in Papua New Guinea, which has practiced cannibalism in the previous, researchers found several folks had a genetic mutation that appeared to guard them from an incurable neurological situation called kuru.
Kuru is caused when people today eat human brain or nervous method tissue that is tainted with an infectious protein and results in symptoms nearly identical to Creutzfeldt-Jakob disease, which humans can contract by eating cows with bovine spongiform encephalopathy, typically referred to as mad cow disease.
Both illness are a form of prion diseases, exactly where an infectious protein causes other proteins to fold in the “wrong” way, eventually top to cell death. Prion diseases usually progress swiftly and are often fatal, according to the U.S. Centers for Disease Control and Prevention.
In an short article published this week in the prestigious journal Nature, researchers revealed they have found a genetic mutation that could possibly protect people from contracting two well-known prion diseases: kuru and Creutzfeldt-Jakob illness.
The genetic variant appears in a huge number of the Fore population and the researches feel that numerous with no the variant may well have died in earlier kuru outbreaks. When kuru was very first identified in the 1950s, up to two % of the Fore population were dying each year from kuru, according to the journal Nature’s web-site.
Researchers replicated the genetic variant they discovered in the Fore population in mice and then infected the mice with either kuru or Creutzfeldt-Jakob. The mice with the identical gene variant as 1 identified in the Fore population appeared to be mostly protected from the disease and its fatal symptoms, researchers located.
Dr. Jiri Safar, co-director of the National Prion Illness Pathology Surveillance Center and associate professor of pathology and neurology at Case Western Reserve University in Cleveland, said the discovering was a “breakthrough” but that much more study would be needed to see if it could be a target for gene therapy.
He said given that the genetic variant was tested in just two forms of prion disease strains, it could not be helpful for other prion-induced illnesses that cause neurological decline.
“It’s quite probable that this protective polymorphism may possibly not be protective across all prion strains,” he explained. “A caveat for the future.”