Jan. 2 (UPI) -- An unnamed drug developed for type 2 diabetes "significantly reversed memory loss" in mice with neurodegeneration similar to Alzheimer's disease, researchers in Britain report in a recent study.
According to Professor Christian Holscher of Lancaster University, lead researcher in the study, the treatment "holds clear promise of being developed into a new treatment for chronic neurodegenerative disorders such as Alzheimer's disease."
Studies have shown people with type 2 diabetes have a higher risk for developing Alzheimer's disease, which is the most common form of dementia and only cause of death in the top 10 that cannot be prevented, slowed or treated, according to the Alzheimer's Association.
More than 5.3 million Americans have Alzheimer's, and that number is projected to grow to 16 million by 2050.
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The drug was referred to only as a "triple receptor agonist," or TA, in the research paper, which was published in Brain Research.
This is the first time that a triple receptor drug was used to protect the brain from degeneration, researchers say.
"With no new treatments in nearly 15 years, we need to find new ways of tackling Alzheimer's," Dr. Doug Brown, director of research and development at the Alzheimer's Society, said in a press release. "It's imperative that we explore whether drugs developed to treat other conditions can benefit people with Alzheimer's and other forms of dementia. This approach to research could make it much quicker to get promising new drugs to the people who need them."
The Alzheimer's Society, based in Britain, helped fund the study.
Although the tests were only conducted on mice, he said it's promising it will help humans, adding that existing diabetes drugs such as liraglutide "have shown real promise for people with Alzheimer's, so further development of this work is crucial."
In the study, mice expressed mutated human genes that cause Alzheimer's were used.
Mice injected with the drug were found to show improved learning and memory formation in a maze. The drug reduced nerve cell loss, the amount of amyloid plaques in the brain linked with Alzheimer's, chronic inflammation and oxidative stress, but enhanced levels of brain growth and slowed down nerve loss.
"These very promising outcomes demonstrate the efficacy of these novel multiple receptor drugs that originally were developed to treat type 2 diabetes but have shown consistent neuro- protective effects in several studies," Holscher said. "Clinical studies with an older version of this drug type already showed very promising results in people with Alzheimer's disease or with mood disorders."
While Holscher said more research is needed, the potential for the drug to help patients is significant.
"Here we show that a novel triple receptor drug shows promise as a potential treatment for Alzheimer's but further dose-response tests and direct comparisons with other drugs have to be conducted in order to evaluate if this new drugs is superior to previous ones," Holscher said.
