How Alzheimer's in Mice Was Reversed in One Week

IL-33 protein repaired cognitive function in mice in only one week, University of Glasgow and Hong Kong University of Science and Technology researchers find.


Could reversing Alzheimer's in just one week be possible soon? New research indicates that might be a real possibility.

In a new study on mice, a protein called IL-33 was found to reverse the cognitive decline and memory issues associated with Alzheimer's in just one week, while appearing to prevent future symptoms as well.

Alzheimer's disease is a type of dementia, or cognitive decline, that can interfere with daily life. About 60 to 80 percent of dementia patients have Alzheimer's disease, a progressive condition that interferes with daily life and eventually causes death.

Symptoms of Alzheimer's disease include memory loss, moodiness, feeling disoriented, difficulty walking and speaking. Most of the five million Alzheimer's patients in the US are over the age of 65 and about one out of three seniors die from some form of dementia or Alzheimer's, according to the Alzheimer's Association.

Scientists from the University of Glasgow discovered that when mice bred to develop cognitive decline as they age were given IL-33, not only did cognitive tasks and memory improve, but physical symptoms of Alzheimer's were also less apparent.

"Previous genetic studies have shown an association between IL-33 mutations and Alzheimer’s disease in European and Chinese populations," co-lead author Eddy Liew, a professor at the university's Institute of Infection, Immunity and Inflammation, said in a press release. "Furthermore, the brain of patients with Alzheimer’s disease contains less IL-33 than the brain from non-Alzheimer’s patients."

Liew co-led the study with professor Nancy Ip of the Hong Kong University of Science and Technology

One physical indicator of Alzheimer's is brain plaque, or an abnormal collection of protein between nerve cells in the brain. Alzheimer's patients also have brain tangles, which are collections of dying nerves. In this study, the mice had less brain plaque after the week of treatment. According to the study authors, IL-33 surrounds the plaque and releases an enzyme to digest it.

Despite the study's results, further studies are necessary to determine how much IL-33 is safe for humans, and Liew advises against too much optimism.

"There have been enough false breakthroughs in the medical field to caution us not to hold our breath until rigorous clinical trials have been done," Liew said. "We are just about to be entering a Phase I clinical trial to test the toxicity of IL-33 at the doses used. Nevertheless, this is a good start.”

This study was published March 15 in the journal PNAS.

The study was financed by the Research Grants Council of Hong Kong SAR, the National Key Basic Research Program of China, the Hong Kong Research Grants Council and the S. H. Ho Foundation.

Researchers declared no conflicts of interest.