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Study Shows That Roche's Investigational Drug for Alzheimer's Disease Removes Amyloid Plaques From the Brain
Date:10/10/2011

fully human anti-A beta antibody, identified and optimized by phage display technology in cooperation with MorphoSys AG, a Munich-based Biotech. It passes the blood-brain-barrier and has a high capacity to specifically bind to cerebral amyloid plaques. While the exact mechanism of antibody-mediated reduction of the amyloid burden is controversial, there is evidence that upon binding of gantenerumab to amyloid plaques brain-resident microglial cells are activated and clear plaques by a process called phagocytosis.

More information on the putative mechanism of the anti-amyloid action of gantenerumab can be found in a recent article entitled "Gantenerumab: A novel human anti-A beta antibody demonstrates sustained cerebral amyloid-beta binding and elicits cell-mediated removal of human amyloid-beta" published by Roche scientists in the Journal of Alzheimer's Disease(2).

About Alzheimer's disease

Alzheimer's disease is the most common form of dementia. Alzheimer's disease is estimated to affect 25 million people around the world with the number of diagnosed cases expected to rise dramatically in the near future(3). It is expected that this illness will affect about 63 million people by 2030, and 114 million by 2050 worldwide(3).

In April 2011, new international guidelines on how to diagnose Alzheimer's were published for the first time in decades(4). These guidelines specifically address how to diagnose Alzheimer's in its earliest stages. They mark a major change in how experts think about and study Alzheimer's, including the need to incorporate biomarker tests.

Roche recently sponsored a website, www.earlysymptomsalzheimers.com , designed to provide healthcare professionals, patients and caregivers with information about prodromal Alzheimer's disease.

About Archives in Neurology

Archives of Neurology is a monthly peer-revie
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SOURCE Roche
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