Experts say they enhanced the learning ability of mice afflicted with a disease alike to Down syndrome by interfering with the making of an exact protein.

The “beta-amyloid” protein is establish in mice and people, the research authors noted, and is considerate to play a position in the cognitive refuse linked with Alzheimer’s and Down syndrome.

The research, announced online June 3 in the journal PLoS One, was conducted using 4-month-old mice that had a genetic irregularity that caused them to display learning disabilities comparable to those in children with Down syndrome.

This beginning research raises the fascinating option that drugs that lower beta-amyloid levels might offer some advantage to children with Down syndrome, study co-author Dr. Craig Powell, a supporter professor of neurology at UT Southwestern Medical Center in Dallas, said in a news release.

The authors indicate that Down syndrome is a genetic illness caused by the attendance of an additional copy of chromosome 21, which leads to the above-normal production of beta-amyloid.

With that in mind, Powell and his colleagues treated young mice with the investigational drug DAPT, which blocks beta-amyloid production by targeting a key enzyme, gamma-secretase.

After four days of action, the mice experienced a 40 percent drop in beta-amyloid levels. In turn, maze navigation tests revealed an development in their aptitude to learn tasks, so that eventually their presentation was deemed as good as that of mice with no genetic impairment.

The experts cautioned, though, that for the time-being this exacting approach is a blunt instrument that blocks not only the targeted enzyme’s ability to spark beta-amyloid production but also a host of other critical assignments the enzyme performs, many of which are central to proper brain meaning.

The team plans to seek out other drugs that might knock out only beta-amyloid creation, while leaving the enyzme’s other functions intact.