Diabetes Drug Reverses Memory Loss in Mice with Alzheimer’s

An experimental drug developed to treat Type II diabetes could be used to treat Alzheimer’s disease after scientists found it “significantly reversed memory loss” in mice through a triple method of action.
Lead researcher Professor Christian Holscher of Lancaster University in the UK said the drug “holds clear promise of being developed into a new treatment for chronic neurodegenerative disorders such as Alzheimer’s disease.”

Alzheimer’s disease is the most common cause of dementia, with the number of people afflicted expected to rise to two million in the UK by 2051, according to the Alzheimer’s Society, which partly funded the research.

“With no new treatments in nearly 15 years, we need to find new ways of tackling Alzheimer’s,” said Dr. Doug Brown, Director of Research and Development at the Alzheimer’s Society. “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.”

“Although the benefits of these ‘triple agonist’ drugs have so far only been found in mice, other studies with existing diabetes drugs, such as liraglutide, have shown real promise for people with Alzheimer’s, so further development of this work is crucial,” he continued.

According to researchers, this is the first time that a triple receptor drug has been used. The drug, which combines GLP-1, GIP, and Glucagon, which are all growth factors, acts in multiple ways to protect the brain from degeneration. Problems with growth factor signaling have been shown to be impaired in the brains of Alzheimer’s patients, researchers noted.

The study used APP/PS1 mice, which are transgenic mice that express human mutated genes that cause Alzheimer’s. Those genes have been found in people who have a form of Alzheimer’s that can be inherited. Aged transgenic mice in the advanced stages of neurodegeneration were treated, the researchers explained.

In a maze test, learning and memory formation were much improved by the drug, according to the study’s findings.

It also enhanced levels of a brain growth factor that protects nerve cell functioning, reduced the amount of amyloid plaques in the brain linked with Alzheimer’s, reduced both chronic inflammation and oxidative stress, and slowed the rate of nerve cell loss, according to the study’s findings.

“These very promising outcomes demonstrate the efficacy of these novel multiple receptor drugs that originally were developed to treat type II diabetes, but have shown consistent neuroprotective 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,” he continued. “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.”

Type II diabetes is a risk factor for Alzheimer’s and has been implicated in the progression of the disease, according to researchers. Impaired insulin has been linked to cerebral degenerative processes in type II diabetes and Alzheimer’s disease.

Insulin desensitization has also been observed in the Alzheimer’s disease brain. The desensitization could play a role in the development of neurodegenerative disorders as insulin is a growth factor with neuroprotective properties, the scientists explain.

The study was published in Brain Research.

Source: Lancaster University http://www.lancaster.ac.uk/