A number of drugs could help protect against Alzheimer’s disease, acting like statins for the brain, scientists say.
In experiments on worms, University of Cambridge researchers identified drugs which prevented the very first step towards brain cell death.
They now want to match up drugs with specific stages of the disease.
According to experts, it was important to find out if these drugs could work safely in humans.
Statins are taken by people to reduce the risk of developing heart disease and the Cambridge research team says its work may have unearthed a potential “neurostatin” to ward off Alzheimer’s disease.
Rather than treating the symptoms of the disease, a neurostatin could be used as a preventative measure to stop the disease appearing in the first place.
Photo Getty Images
The cancer drug bexarotene, for example, was found to stop the first step which leads to the death of brain cells in worms genetically programmed to develop Alzheimer’s disease.
In previous trials in humans, researchers tested the drug at a later stage of the disease to see if it would clear amyloid plaques from the brain but the trials were unsuccessful.
Writing in Science Advances, Prof. Michele Vendruscolo, senior study author from the University of Cambridge, said the research team wanted to find out more about the mechanics of every stage of the disease’s development.
“The body has a variety of natural defenses to protect itself against neurodegeneration, but as we age, these defenses become progressively impaired and can get overwhelmed.
“By understanding how these natural defenses work, we might be able to support them by designing drugs that behave in similar ways.”
The first details of how Eli Lilly’s solanezumab drug could slow the pace of brain decline for patients with early stage Alzheimer’s disease have emerged.
Data from pharmaceutical company Eli Lilly suggests its drug can cut the rate of the dementia’s progression by about a third.
The results, presented at the Alzheimer’s Association International Conference in the US, are being met with cautious optimism.
A new trial is due to report next year and should provide definitive evidence.
The death of brain cells in Alzheimer’s is currently unstoppable. Solanezumab may be able to keep them alive.
Current medication, such as Aricept (Donepezil), can manage only the symptoms of dementia by helping the dying brain cells function.
But solanezumab attacks the deformed proteins, called amyloid, that build up in the brain during Alzheimer’s.
It is thought the formation of sticky plaques of amyloid between nerve cells leads to damage and eventually brain cell death.
Solanezumab has long been the great hope of dementia research, yet an 18-month trial of the drug seemingly ended in failure in 2012.
However, when Eli Lilly looked more closely at the data, there were hints it could be working for patients in the earliest stages of the disease.
It appeared to slow progression by around 34% during the study.
So the company asked just over 1,000 of the patients in the original trial with mild Alzheimer’s to take the drug for another two years.
Positive results from this extension of the original trial have now been presented at the Alzheimer’s Association International Conference.
They show those taking the drugs the longest had the most benefit.
Eli Lilly also started a completely separate trial in mild patients in 2012, and these results could prove to be the definitive moment for the drug.
In the first stage of the original trial, which ended in failure, half of the patients with Alzheimer’s were given solanezumab and half were not.
A reanalysis of the cognition scores of the patients with mild Alzheimer’s suggested taking the drug had cut the rate of the disease’s progression by about 34%.
The implication is that the amount of cognitive decline normally seen in 18 months would take 24 months with the drug.
In the extension of the original trial, all of the 1,000-plus mild Alzheimer’s patients participating were given solanezumab.
At the end of the extension, half of them had been taking the drug for three and a half years while the other half had been taking it for two years.
The latest data shows those taking solanezumab for the longest time still had better scores of cognitive function.
This suggests the course of the disease was being slowed.
If the patients’ brains had continued to decline at the normal pace and the drug had been merely helping with symptoms, then all of the patients participating in the extension of the original trial – whether they had been taking solanezumab for three and a half or two years – would have had similar scores of cognitive function.