For decades, intensive research has been conducted on drugs all over the world to treat Alzheimer's patients. Although major progress has been made in diagnostics (the disease can be detected increasingly early and accurately), the therapeutic options remain limited. Together with researchers in Switzerland, Germany and India, a team headed by Professor Lawrence Rajendran from the Systems and Cell Biology of Neurodegeneration at the Institute of Regenerative Medicine of the University of Zurich has now developed a targeted substance that blocks the pathogenic function of an enzyme (beta-secretase) in cells without affecting the enzyme’s other vital functions. The new work was published online on February 25, 2016 in the journal Cell Reports. The open-access article is titled “Specific Inhibition of β-Secretase Processing of the Alzheimer’s Disease Amyloid Precursor Protein.” Protein deposits in the brain are hallmarks of Alzheimer's disease and are partly responsible for the chronically progressive necrosis of the brain cells. Nowadays, these plaques can be detected at very early stages, long before the first symptoms of dementia appear. The protein clumps mainly consist of the β amyloid peptide (Aβ), a protein fragment that forms when two enzymes, β and γ secretase, cleave the amyloid precursor protein (APP) into three parts, including Aβ, which is toxic. If β or γ secretase is blocked, this also inhibits the production of any more harmful Aβ peptide. Consequently, for many years, biomedical research has concentrated on these two enzymes as therapeutic points of attack. To date, however, the results of clinical studies using substances that block γ secretase have been sobering. The problem is that the enzyme is also involved in other key cell processes.
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