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Keywords:

  • Alzheimer's disease;
  • amyloid-beta protein;
  • immunotherapy;
  • protofibrils;
  • transgenic mice

The identification of disease-causing mutations in Alzheimer's disease has contributed greatly to the understanding of the pathogenesis of this disease. The amyloid-β (Aβ) peptide has come into focus and is believed to be central to the pathogenesis of Alzheimer's disease. With only symptomatic treatment available, efforts to develop new therapeutics aimed at lowering the amount of Aβ peptides in the affected brain have intensified. In particular, immunotherapy against Aβ peptides has attracted considerable interest, as it offers the possibility to generate highly specific molecules targeting highly specific moieties. Due to intense research efforts and massive investments at universities and in the pharmaceutical industry, the outlook for patients and their relatives has never been brighter.