A drug developed for type 2 diabetes significantly reverses memory loss and could have potential as a new treatment for Alzheimer’s disease and other neurodegenerative diseases, scientists say.
The study, by UK and Chinese universities, is the first to look at a new combined diabetes drug and found improvements in several characteristic symptoms of Alzheimer’s.
Lead researcher Professor Christian Holscher, from Lancaster University, said these “very promising outcomes” show multi-action drugs developed for type 2 diabetes “consistently show neurological protective effects”.
Independent academics said a reduction in nerve-cell-killing protein molecules was particularly interesting and this was likely to be another avenue in the search for an elusive drug to combat dementia.
He has previously reported optimistic findings from an older diabetes drug, liraglutide, and clinical trials in humans are currently under way.
This latest study, published in the journal Brain Research, looked at a “triple action” treatment that combine three different drugs for type 2 diabetes, acting on biological pathways that could also have an impact on dementia.
Type 2 diabetes is a known risk factor for Alzhemier’s disease and impaired production of insulin – the hormone that people with diabetes don’t produce sufficiently to control their blood sugar – is linked to brain degeneration.
The identification of this link had a twofold benefit, according to charities.
It opened up new research and drug development opportunities, such as this study.
But it also means that by making lifestyle changes, like eating healthily and exercising, patients can avoid developing type-2 diabetes and lower their risk of Alzheimer’s disease as well.
There are currently half a million people living with Alzheimer’s disease in the UK and more than five million people with diabetes, both conditions pose a major cost to the NHS, and health systems worldwide.
The treatment in this study combined; GLP-1, GIP and glucagon, which, like insulin protect against neurological deterioration, and tested them in mice with genetic mutations that cause Alzheimer’s disease.
After two months of daily injections the mice were shown to significantly improve their performance in a maze designed to test memory.
Treated mice also had lower levels of proteins which clump together and form plaques in the brains of people with Alzheimer’s disease, inhibiting nerve cells’ ability to communicate and causing them to die.
The study also found these mice lost nerve cells to the disease at a slower rate and had lower levels of nerve inflammation.
It concludes that the triple treatment “holds clear promise of being developed into a new treatment for chronic neurodegenerative disorders such as Alzheimer’s disease”.
The Alzheimer’s Society, a charity which part-funded the latest study research, said that after 15 years without a new drug for Alzheimer’s disease the promising results from these crossover treatments, which are already known to be safe for humans, are likely to bring earliest benefits.
Professor Holscher added that further tests to compare its benefits against other potential treatments, and its effects in humans were needed.
But Professor John Hardy, a professor of neuroscience, at University College London who was not involved in the trial, said the study was “a first step, at best” towards a Alzheimer’s drug for humans.
“The results showing less amyloid deposition of amyloid in mice treated with glucagon receptor stimulating drugs is interesting,” he said.
“However, it should be noted that several other drugs have shown positive results in mice models of Alzheimer’s disease and then failed in human trials.”
Dr David Reynolds, chief scientific officer at Alzheimer’s Research UK, echoed this, but added: “There is a long road between studies that show an effect in animals and treatments in the hands of patients, and scientists will only be able to realise the potential of promising findings like these if we continue to invest in research.”
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