Introduction: The amyloid hypothesis states that Abeta is the main trigger for Alzheimer's disease. This report is focused in the study of the processing of the Amyloid Precursor Protein (APP) as a procedure to investigate the molecular mechanisms that may result in changes in the levels of Abeta.
Methods: Here we analyse different methodologies for Abeta determination, soluble APP, APP-Carboxy terminus fragments (CTFs) and enzymes for synthesis (secretases) and degradation of Abeta. In addition the advantages and disadvantages of different methodologies are discussed.
Discussion: The potential value of these procedures is described in the context of the function of APP and the different fragments derived from its cleavage.
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