ABSTRACT
Despite intense efforts, it has not yet been possible to clarify the etiopathogenesis, multigenic and multifactorial in character, of Alzheimer’s disease (AD). AD is mainly characterized by the presence of two types of brain lesions consisting of the paired helical filaments (PHF) of proteinaceous material in neurons and amyloid deposits in the extracellular space. The main component of amyloid, called ßA4 and formed by a chain of 39-43 amino acids, derives from a much larger transmembrane glycoprotein (Figure 1) which accumulates in diffuse and mature plaques associated with the neurodegenerative process.
