Washington ? A rare disorder that turns children into old people and often causes them to die in their teens has been linked to a single genetic mutation, a finding that may help science learn more about normal aging as well.

The disorder, called Hutchinson-Gilford progeria syndrome, is caused by a single “misspelling” or misplaced DNA molecule within the human genome that contains some 3 billion DNA units, said Dr. Francis Collins, head of the National Human Genome Research Institute and the senior author of a report appearing this week in the journal Nature.

Victims of progeria appear normal at birth, but by 18 months begin to develop symptoms of accelerated aging. The skin takes on the appearance of the elderly, bones become fragile and most of the children are bald by the age of 4. The children never grow much taller than three feet. Their internal organs also quickly age, and death is usually caused by heart disease or stroke at an average age of 13.

Even as teenagers, said Dr. W. Ted Brown, the children with progeria will weigh only 30 to 35 pounds.

Children with the disorder, however, tend to have above-average intelligence, said Brown, a co-author who has studied progeria for 20 years at the New York State Institution for Basic Research in Development Disabilities.

Progeria affects only about one baby per 4 million to 8 million worldwide, according to the Progeria Research Foundation.

The disease was first identified in 1886, but Brown said it has been difficult to study because “there are only a handful or so alive at one time.” He said about one patient with progeria is born each year in the U.S.

In the study, Collins said researchers looked at the genetic complement of 20 progeria patients and their parents. He said they found 18 of the patients shared the same mutation in the LMNA gene on Chromosome 1.

The flaw, he said, was a substitution of single DNA base. The amino acid guanine is switched to adenine.

Collins said that the next step for progeria researchers was to find a drug that corrected the specific flaw from the mutate LMNA gene. Eventually, it may be possible to correct the gene itself, he said.

But Collins said researchers also were going to now look at people who live to be very old see if the is some element of their LMNA gene that makes them resistant to the diseases of aging.