A cancer drug used to strengthen the human body's immune system against tumor has been found to have the ability to reduce the buildup of Alzheimer's-related plaques by 50 percent and restore certain memory functions in mice.

Although it is still a long way before the results of the finding make its way from mouse models to human beings, they could help scientists learn more about the complex relationship between the human immune system and the cause of dementia. Scientists had long suspected that the brain's overactive immune system could be the culprit.

Many scientists believe that calming down the overactive brain system will be a useful treatment for the disease. However, drugs aimed at doing this, called anti-inflammatories, have not had much success in clinical trials," said Tara Spires-Jones from the University of Edinburgh who was not involved in the research.

The team of researchers, led by Kuti Baruch from the Weizmann Institute of Science in Israel, worked with genetically engineered mice (called the 5XFAD mouse model) that have the ability to express the mutated version of the human amyloid precursor protein (APP) to conduct their study. AAP is a membrane protein that is expressed in many tissues and is concentrated in the synapses of the neurons. Scientists, however, have not unraveled yet what exactly this protein does.

AAP, though, is linked to the production of beta amyloid that forms the toxic amyloid plaques found in patients suffering from Alzheimer's disease.

The mice, which were displaying Alzheimer's-related plaque buildup and memory loss, were given an FDA-approved class of drugs called PD-1 immune checkpoint blockades. The results showed that the plaques were cleared by up to half the original amount. More so, the mice displayed a memory regain as they were able to go through a maze.

The findings are published in Nature Medicine.