A team of scientists in South Korea have found a way to remove toxic plaques from the brains of mice with Alzheimer’s disease, resulting in an improvement in the animals’ cognitive function and memory-forming abilities. While the researchers are remaining cautious about the implications of their work – since results obtained in laboratory mice don’t always translate to humans – their findings could well shed light on a major cause of Alzheimer’s and suggest a potential pathway for treatment.

According to the study, which appeared in the journal Nature Communications, Alzheimer’s disease is typically accompanied by the formation of plaques around the gaps between nerve cells in the brain, across which signals are transmitted. These plaques are generated when amyloid-beta proteins group together. While the exact means by which this causes the condition is not known, several studies have indicated a strong correlation between the build-up of these amyloid plaques and neuronal dysfunction.

In an attempt to investigate the importance of these plaques in Alzheimer’s, the team behind the study sought a means of removing them from the brains of mice bred to have the condition. To do so, they laced the mice’s drinking water with a small molecule called 4-(2-hydroxyethyl)-1-piperazinepropanesulphonic acid (EPPS), which is known to bind to amyloid-beta aggregations and break them down into single-unit proteins again.

The researchers discovered that mice that orally received EPPS performed much better than those that didn't when placed in a Y-shaped maze, suggesting that the break-down of these plaques may serve to enhance short-term working memory in Alzheimer’s sufferers. To confirm that this improved cognitive behavior corresponded to a removal of amyloid plaques, the scientists later removed the brains of the mice, noting that those that had received EPPS did indeed contain far fewer plaques than the control group.

As such, the team has stated that its experiment “provides strong support for the view that the accumulation of amyloid-beta is an important mechanism underlying Alzheimer’s disease.” The researchers subsequently suggest that “interventions specifically aimed at disaggregating existing plaques... may constitute a useful approach to [Alzheimer’s] treatment.”

However, while the study and its findings have been well received, some experts warn it is too early to jump to conclusions about its potential in the battle against dementia. For instance, Professor Tom Dening of the University of Nottingham told the BBC that “from a clinician's point of view, this research is of interest, but we still don't know if removing amyloid plaques is useful in humans