Sky News: A cure for Alzheimer’s could soon become a reality following trials of a drug that fights sticky deposits in the brain linked to the disease.
According to a leading charity the research provides “tantalising evidence” Alzheimer’s could become treatable with the antibody ‘aducanumab’.
Although currently available treatments can help reduce symptoms of the disease, there has until now been nothing which can halt or slow its progress.
The findings will bring hope for the estimated 850,000 people in the UK that suffer from some form of dementia, most having Alzheimer’s. By 2025 their numbers could increase to more than a million.
The primary cause of brain deterioration underlying Alzheimer’s is thought to be sticky deposits of beta-amyloid, a protein found in the fatty membrane surrounding nerve cells.
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 it 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.
The clinical trials involved patients receiving monthly infusions of aducanumab or a placebo for one year.
Scans showed that patients given the antibody showed a greater reduction in beta-amyloid.
Dr 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.”
Recruiting of patients for bigger trials has already started.
