One possibility can be that Aβ accumulation — the buildup of Aβ in various forms, including soluble Aβ, oligomeric species, or amyloid plaque deposition — For example, studies have shown that Aβ accumulates in the cortexmay be the result of a protective response rather than the cause of the pathology, and therefore amyloid peptide treatment would not produce the desired results, hence leading us to question the relevance of models based on APP overexpression or Aβ administration248 and calling for principally new models of AD. The gene discussed is APP; the disease is Alzheimer disease.