Experts are taking care not to build up false hopes about the antibody drug, aducanumab, which clears away sticky protein fragments in the brain linked to Alzheimer’s.
However, David Reynolds, chief scientific officer at Alzheimer’s Research UK, said: “These results provide tantalising evidence that a new class of drug to treat the disease may be on the horizon.
“The findings suggest that aducanumab may slow memory and thinking decline in people with early Alzheimer’s and, although the analysis is only exploratory in this early trial, it paints a positive picture for ongoing trials with the drug,” said Dr Reynolds.
Current treatments can reduce symptoms to some extent but doctors have nothing that can halt or slow progression of the disease.
According to the Alzheimer’s Society of Ireland, there are almost 48,000 people living with dementia in Ireland. Around 4,000 of these people are under 65 and are classified as having younger onset dementia. It is estimated that the number of people living with dementia will rise to 153,157 by 2046 due to our ageing population.
Alzheimer’s is linked to the build up of sticky clumps of beta-amyloid peptide — pieces of protein — in the brain.
Beta-amyloid toxicity is thought to be a primary cause of the neural dysfunction and degeneration which underlies the disease.
Scientists have long known that removing beta-amyloid could lead to a glittering prize — halting or at least slowing Alzheimer’s progression. But until now all attempts to target the peptide with a drug have met with failure.
Aducanumab is a monoclonal antibody — an immune system agent copied and produced in a laboratory which selectively targets beta-amyloid.
Tests on mice genetically engineered to develop a disease similar to Alzheimer’s showed that the drug could enter the brain and reduce levels of beta-amyloid in a dose-dependent fashion.
Scientists also conducted an early Phase I trial to evaluate the safety and tolerability of monthly aducanumab injections in patients displaying early symptoms of Alzheimer’s disease.
A total of 165 patients received monthly infusions of either aducanumab or a placebo “dummy drug” for one year. After 54 weeks of treatment, scans showed that levels of beta-amyloid had been significantly reduced in the brains of patients given the antibody. Higher doses were associated with greater reduction, the researchers reported in the journal.
At the higher doses, removal of beta-amyloid was also associated with slower mental decline. However, the preliminary study was not designed to assess aducanumab’s clinical effectiveness, which will now have to be tested in larger trials.