Injection of an immune signaling protein into mice seem to
reverse the effects of Alzheimer’s disease progression, reported a team at the University of Glasgow. While experimental and only tested in mice, the team is cautiously optimistic about the clinical applications of this treatment for the increasing number of patients suffering from Alzheimer’s disease.
The protein is called interleukin 33 (IL-33), and is produced naturally part of the body’s immune defense mechanism. Its expression is highest in the brain and the spinal cord. Interestingly, scientists found that brains of Alzheimer’s patients have lower amounts of IL-33 as compared to healthy adults. Thus, a team from the University of Glasgow and the Hong Kong University of Science and Technology sought to investigate whether IL-33 could rescue some Alzheimer symptoms.
For their study, they used a mouse model of Alzheimer known as APP/PS1, which show progressive neurodegeneration as seen in Alzheimer patients. Half of the mice received IL-33 injections in the abdomen while the other half received placebo injections. After a week, the team measured changes in cognitive decline between the two groups.
They found mice treated with IL-33 showed improved memory and cognitive functions compared with the control group. This included tests for learning, memory, response to stimulus, and retrieval abilities. In addition, they also found IL-33 treated brains showed evidence of reduced amyloid plaques, which are the hallmark feature of Alzheimer’s disease.
How does an immune protein improve symptoms of a neurodegenerative disease like Alzheimer’s? The team thinks IL-33 may stimulate other immune cells to break up or destroy the toxic amyloid clusters. IL-33 may also dampen the body’s inflammatory response that would otherwise drive formation of new amyloid clusters.
But the exact mechanisms behind these results are still being fleshed out. In addition, the team cautions that the results are preliminary and only in mice. "Exciting as it is, there is some distance between laboratory findings and clinical applications. 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," said Eddy Liew, Professor at the University of Glasgow and co-author of the study.
Animal studies such as this are essential before a treatment makes it way to human clinical trials. But it is not uncommon for a drug to behave differently in humans than it did in animal tests. The team hopes this will not be the case for IL-33, and they hope to have some answers in the next five years.
"The role of the immune system in Alzheimer's disease and other causes of dementia is a promising area of focus for drug discovery efforts. This early research in mice highlights a way of boosting the immune system to clear a toxic Alzheimer's protein, but we'll need to see the results of clinical trials before we'll know whether this approach could one day help people living with the disease," said Simon Ridley, Director of Research, Alzheimer's Research UK.
Additional sources:
BBC,
NHS UK
