Discovery allows scientists to block Alzheimer's
Scientists developing treatments for the devastating brain disorder Creutzfeldt-Jakob Disease (CJD) have unexpectedly blocked the onset of Alzheimer's disease, the most common cause of dementia.
Researchers said they were "thrilled" at the unexpected discovery that two antibodies – extensively studied in relation to CJD – may also have an affect on Alzheimer's disease. Almost 500,000 people a year in the UK and 20 million worldwide suffer from Alzheimer's.
The finding, published in Nature Communications, represents a "significant step forward in the battle to develop drugs to treat Alzheimer's disease," they say. The lead came from an American study by researchers at Yale University in 2009, which showed prion proteins causing CJD also play a role in Alzheimer's disease.
The finding triggered a race by scientists to discover whether antibodies being developed as a treatment for CJD might also work against Alzheimer's. Now a study on mice at the Medical Research Council Prion Unit at University College London has indicated the antibodies block the damaging effects of a toxic substance called "amyloid beta", a protein which accumulates and becomes attached to the nerve cells in the brain.
Over time, through its interaction with prion proteins, amyloid stops the nerve cells from communicating, causing memory loss, the distinctive symptom of Alzheimer's.
Professor John Collinge, the director of the MRC Prion Unit at University College London who led the study published in Nature Communications, said: "There is an urgent need for new drugs which will help to preserve brain function and prevent memory loss, the symptom which most characterises the devastating impact of Alzheimer's. We're thrilled that this discovery shows in mice that these two antibodies which we are developing to treat CJD may also have a role in treating more common forms of dementia like Alzheimer's disease.
"If these antibody drugs prove to be safe in use to treat CJD we will consider whether studies in Alzheimer's disease should be carried out."
Professor Dominic Walsh, a co-author of the study from University College Dublin, said: "A unique aspect of this study is that we used amyloid beta extracted from human brain, the same material we believe is causing memory loss in patients with this devastating disease and we identified two antibodies that could block this effect.
"The use of these specific antibodies is particularly exciting since they have already undergone extensive pre-clinical testing for use in treating CJD. Thus a lot of basic work has already been done and could fast-track these antibodies for use in humans. The next step is further validation in other disease models of Alzheimer's and then safety trials in humans."
The two antibodies, ICSM 18 and 35, target the prion protein that is implicated as a cause of CJD. Clinical trials of drugs based on the antibodies are due to begin in humans next year as a treatment for CJD. If they are successful, the trials could be repeated for patients with Alzheimer's disease.
One in 14 adults over aged 65 and one in six over aged 80 has dementia, which in most cases is Alzheimer's disease. The incidence is growing as the population ages.