RESUMEN
N-terminal truncated amyloid beta (Aß) derivatives, especially the forms having pyroglutamate at the 3 position (AßpE3) or at the 11 position (AßpE11) have become the topic of considerable study. AßpE3 is known to make up a substantial portion of the Aß species in senile plaques while AßpE11 has received less attention. We have generated very specific polyclonal antibodies against both species. Each antibody recognizes only the antigen against which it was generated on Western blots and neither recognizes full length Aß. Both anti-AßpE3 and anti-AßpE11 stain senile plaques specifically in Alzheimer's disease cerebral cortex and colocalize with Aß, as shown by confocal microscopy. In a majority of plaques examined, AßpE11 was observed to be the dominant form in the innermost core. These data suggest that AßpE11 may serve as a generating site for senile plaque formation.