Those responsible for developing the model were the working group of Prof. Dr. Thomas Willnow, the biomathematician Dr. Jana Wolf from the MDC and systems biologists from the University of Rostock. The starting point of their model calculation was the transport molecule SORLA, which is produced by the nerve cells. This molecule influences the production of the harmful protein plaques in the brain characteristic of Alzheimer’s disease. These plaques in the brains of Alzheimer’s patients are made up of protein fragments – so-called amyloid beta peptides - which derive from an amyloid precursor protein and are deposited in the brain over the course of many years, destroying the patients’ nerve cells and leading to mental decline.

Prof. Willnow and his Berlin colleagues compared the brains of humans who had died of Alzheimer’s disease with those of humans who had not suffered from the disease. The scientists identified a genetic variant of SORLA which occurred more often in the brains of Alzheimer’s patients than in the healthy brains. This genetic variant causes nerve cells to produce significantly less SORLA than would  normally be the case. The unhindered production of amyloid beta peptides in the brain of humans as a result of low SORLA production may lead to the Alzheimer’s disease in later life.

Prof. Willnow stressed in an interview that for ethical reasons it is only sensible to use such models to identify risk patients as candidates for early treatment when there is actually a therapy for Alzheimer’s. And this is still being worked on by researchers around the world.

Source: http://idw-online.de/

Original Literature: Schmidt, V. et al. (2011): Quantitative modeling of amyloidogenic processing and its influence by SORLA in Alzheimer’s disease. EMBO, doi:10.1038/emboj.2011.352.