WEDNESDAY, May 3, 2017 (HealthDay News) -- A gene mutation seems to speed up the loss of memory and thinking skills in people with Alzheimer's disease, new research suggests.
Researchers said the gene mutation -- called BDNF Val66Met allele, or the Met allele -- was pinpointed by following more than 1,000 people who were at risk of developing Alzheimer's disease. The researchers followed them for 13 years. The participants' average age was 55 at the start of the study.
Blood samples were tested for the gene mutation. Memory and thinking abilities were tested at the start of the study and at up to five visits during the study period.
The 32 percent of participants with the Met allele lost memory and thinking skills more rapidly than those without the gene mutation, the findings showed. The decline was even quicker among those with both the Met allele and higher levels of beta-amyloid, a sticky protein that can form plaques in the brains of people with Alzheimer's disease.
The BDNF gene normally produces a protein that helps nerve cells grow, specialize and survive.
"Because this gene can be detected before the symptoms of Alzheimer's start, and because this presymptomatic phase is thought to be a critical period for treatments that could delay or prevent the disease, it could be a great target for early treatments," said study author Ozioma Okonkwo of the University of Wisconsin School of Medicine.
"When there is no mutation, it is possible the BDNF gene and the protein it produces are better able to be protective, thereby preserving memory and thinking skills," Okonkwo said in a news release from the American Academy of Neurology.
"This is especially interesting because previous studies have shown that exercise can increase levels of BDNF. It is critical for future studies to further investigate the role that the BDNF gene and protein have in beta-amyloid accumulation in the brain," Okonkwo concluded.
The study was published online May 3 in the journal Neurology.
SOURCE: American Academy of Neurology, news release, May 3, 2017