The amyloid peptide (A) represents another widely
studied extrinsic pathologic inducer of neuronal apoptosis
(Carter and Lippa, 2001; Mattson et al., 1998; Yankner et al.,
1989). The amyloidogenic 42-amino acid A peptide is generated
through aberrant processing of the amyloid precursor
protein (APP). A is the primary component of senile
plaques that are prevalent in the brains of AD, the most common
neurodegenerative disease (Hardy and Selkoe, 2002).
Although controversy has surrounded the understanding of
the role of A in the pathogenesis of AD (Neve, 2001), both
in vitro and in vivo evidence suggests that exposure of neurons
to A induces apoptosis