Kuru is the earliest human prion disease to be studied. Prions are different from any pathogenic microorganisms that humans have discovered so far that use nucleic acid replication as a genetic basis. They are protein infectious particles that lack nucleic acids and can proliferate on their own without nucleic acid replication. Kuru is only seen in the Fore tribe in the eastern plateau of New Guinea, with a population of only 30,000 to 40,000. Due to participating in religious rituals of cannibalism, more than 200 people died of tremors and a disordered walking within a year. Locals call this Kuru. Kuru has a long incubation period, ranging from 4 to 30 years, and the onset is insidious. Patients in the prodromal stage only feel headaches and joint pain, followed by ataxia, tremors, and involuntary movements. The latter include chorea, myoclonus, etc., and progressive dementia and neurological abnormalities appear in the late stage of the disease. In view of the many similarities between Kuru brain changes and sheep scrapie, Gajdusek of the US NIH ground Kuru brain and inoculated it into the brain of orangutans. The animals became ill 13 months later. He believed that the pathogen of the disease was a special type of slow virus, called an unusual slow virus. Currently, it is believed that the disease is a transmissible neurodegenerative disease caused by mutant prion protein, also known as prion disease or protein particle disease. This denies the unusual slow virus infection theory advocated by Gajdusek many years ago.