A collaboration between researchers at University of Ulster and Lancaster University has investigated whether drugs used in the treatment of type 2 diabetes may protect nerve cells from damage associated with Alzheimer’s in mice bred to develop signs of the disease. The scientists used mice that produce large quantities of a protein called amyloid, known to build-up in Alzheimer’s, in order to replicate in mice some of the hallmarks of the condition seen in humans. One group of mice was treated with a diabetes drug called Lixisenatide, while a second was treated with another diabetes drug called Liraglutide. In order to compare the effects of the drugs, a third group of mice received no treatment at all.
The researchers found that after 10 weeks of daily treatment, the treated mice performed better on a type of memory test that involves object recognition. They found that the drug treatments reduced the amount of amyloid in the brain and dampened brain inflammation, which is thought to play a role in nerve cell damage. The scientists also looked at nerve cells themselves and found that the diabetes drugs increased the number of communication points and strengthened connections between neighbouring nerve cells. Lixisentatide was the most effective when it came to strengthening communication between nerve cells.
Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said: “Diabetes is a known risk factor for Alzheimer’s although we still do not fully understand the mechanisms linking the two conditions. Previous laboratory research has suggested that some treatments for type 2 diabetes could help to protect the brain from the damage caused by Alzheimer’s disease.
"This study found that two diabetes drugs could slow nerve cell damage in mice with some of the hallmarks of Alzheimer’s and that the animals also performed better on a memory test. While this study does highlight an interesting target for the development of new treatments for the disease, the next important step will be to see whether these benefits seen in mice can be reproduced in clinical trials in people.”
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