It is the first time that clinical data has been published for gantenerumab, an investigational compound with a mechanism of action targeted at the early stages of Alzheimer’s disease.

Results from Phase I clinical trials and ex vivo studies demonstrated that gantenerumab treatment results in a dose-dependent reduction of brain amyloid, possibly through phagocytosis through brain microglial cells, whereas amyloid load increased in patients receiving placebo treatment.

“These results and especially the rapidity of the effects observed on amyloid removal are very encouraging and pave the way for the development of a novel treatment for Alzheimer’s disease,” said Luca Santarelli, Global Head of Roche Neuroscience Disease Translational Area. “Our approach is to utilise biomarkers to diagnose and treat the disease at a very early stage before significant damage to the brain has occurred.”

Gantenerumab is an investigational fully human anti-amyloid monoclonal antibody designed to bind to amyloid plaques in the brain and remove them. It is hoped that this approach will slow progression of the disease, an outcome that cannot be achieved with currently approved treatments.

“Our objective was not only to demonstrate the effects of gantenerumab on brain amyloid, but also to start elucidating its mechanism of action,” added Santarelli, “this is extremely important to fully understand the compound’s therapeutic potential for Alzheimer’s disease.”

Since it is known that amyloid accumulates in patients’ brains about 15 years before the onset of dementia, ongoing and future clinical studies with gantenerumab will focus on Alzheimer’s disease in the early or prodromal phase. It is hoped that early diagnosis and intervention, before significant damage to nerve cells has occurred, will offer optimal benefit to patients.

The study ‘Mechanism of amyloid removal in patients with Alzheimer disease treated with gantenerumab’ is published in the October issue of Archives in Neurology.