Anti-Alzheimer’s drug trial success brings hope of cure

10^th October 2013

Camilla Capasso

Camilla Capasso

10 October 2013

A British study published on Science Transnational Medicine suggests a drug-like compound could treat brain diseases such as Alzheimer and Parkinson. Indeed, research carried out on sick mice found that the compound stops the degeneration of brain cells.

Five weeks after the treatment, one group of mice remained free of symptoms such as memory loss. They also lived longer than untreated animals with the same disease. The experimental drug, known as GSK2606414, is made by pharmaceutical company GlaxoSmithKline.

Experts say the result could be a turning point although it could take almost a decade before any medicine is developed.

Professor Giovanna Mallucci, the Medical Research Council (MRC) scientist who led the team of researchers, said: “We were extremely excited when we saw the treatment stop the disease in its tracks and protect brain cells, restoring some normal behaviours and preventing memory loss in the mice.”

However, Ms Mallucci pointed out that, despite protecting the brain, the compound has also some side effects like weight loss and mild diabetes.

The MRC team focused on the main cause of many degenerative brain diseases such as Alzheimer and Parkinson that are caused by abnormally shaped proteins that stick together in clumps and fibres.

When enough proteins build up in the brain, it causes the activation of a natural defence mechanism in cells, switching off the production of new proteins. The production of proteins should normally switch on again but, in the case of Alzheimer and Parkinson, it doesn’t, causing the death of nerve cells.

Researchers have found that the compound used in GSK2606414 can switch on the protein production again, stopping the degeneration of brain cells.

Professor Hugh Perry, chair of the MRC’s neuroscience and mental health board showed his enthusiasm for recent the discovery: “Despite the toxicity of the compound used, this study indicates that, in mice at least, we now have proof-of-principle of a therapeutic pathway that can be targeted.”

Camilla Capasso