Alzheimer's drug results wow conference
An experimental drug has been shown to reduce amyloid beta build-up and slow cognitive decline in early Alzheimer’s.
The results from the phase 1b trial caused excitement at the 12th International Conference on Alzheimer’s and Parkinson’s Disease held in Nice, France, and sent stock in its maker Biogen soaring to an all-time high.
“It’s a major advance in confirming amyloid beta is the right target,” Professor Colin Masters of the University of Melbourne and the Florey Institute of Neuroscience and Mental Health told Bloomberg.
Professor Masters, who attended the conference and was not involved in the trial, has been studying Alzheimer’s disease for over 30 years.
The trial involved 166 patients with prodromal AD and PET-confirmed amyloid beta deposition. They were randomised to monthly injections of placebo or various doses of the monoclonal antibody aducanumab, over 54 weeks.
At week 26, patients taking aducanumab had a dose-dependent reduction in amyloid plaque in all six brain regions identified as of interest.
Reductions were even greater at 54 weeks, and were also higher with larger doses of the drug.
While the performance of all patients worsened in cognitive tests during the course of the trial, the decline was much steeper in those taking placebo. The researchers also found those who had the largest dose of aducanumab had the smallest decline in cognitive function.
However, adverse effects were associated with the drug, particularly fluid build-up around the blood vessels. Over 20% of patients taking drug experienced headaches, compared with 5% in the placebo group.
On the basis of the results, Biogen will proceed directly to a phase 2 trial enrolling 1,000 patients, a Biogen spokesperson confirmed.
Alzheimer’s drug research has been in the doldrums lately, with a series of drugs showing promise in early trials, only to flop at phase 3.
Many researchers now believe these drugs were trialled too late in the disease process, when severe, irreversible brain damage had already occurred. The trials may also have been confounded by participants who had non-Alzheimer’s dementia, in which amyloid plaque build-up was not implicated.
The current trial got around some of these problems by enrolling patients with mild, early forms of the disease and confirming baseline plaque build-up through imaging.
No drug is currently marketed to slow, stop or reverse the progress of Alzheimer’s disease.
Reproduced from 6minutes 27/3/15
