Pathological changes typical of Alzheimer's were considerably reduced in mice by blockade of an immune system transmitter, promising potential in prevention, as well as in cases where the disease has already set in.
The finding by Charite - Universitatsmedizin Berlin and the University of Zurich suggest that accumulation of particular abnormal proteins, including amyloid-beta among others, in patients' brains plays a central role in this disease.
Alzheimer's disease is one of the most common causes of dementia. In Germany and Switzerland alone, around 1.5 million people are affected, and forecasts predict a doubling of the number of patients worldwide within the next 20 years.
Professors Frank Heppner and Burkhard Becher were able to show that turning off particular cytokines (immune system signal transmitters) reduced the Alzheimer's typical amyloid-beta deposits in mice with the disease.
As a result, the strongest effects were demonstrated after reducing amyloid-beta by approximately 65 per cent, when the immune molecule p40 was affected, which is a component of the cytokines interleukin (IL)-12 and -23.
Follow-up experiments also relevant for humans showed that substantial improvements in behavioural testing resulted when mice were given the antibody blocking the immune molecule p40.
This effect was also achieved when the mice were already showing symptoms of the disease.
The level of p40 molecules is higher in Alzheimer's patients' brain fluid, which is in agreement with a recently published study by American colleagues demonstrating increased p40 levels in blood plasma of subjects with the disease, thus showing obvious relevance for human therapy.
Researchers suspect that cytokines IL-12 and IL-23 themselves are not causative in the pathology, and that the mechanism of the immune molecule p40 in Alzheimer