[Abstract Title]. - Society for Neuroscience

pGluAbeta(3-42). The isolated regulated secretory vesicles contained substantial levels of
pGluAbeta, combined with Abeta40 and Abeta42. Each of these Abeta peptide forms were
present at similar levels. Furthermore, these Abeta peptides are colocalized in these RSV with
multiple peptide neurotransmitters and catecholamines, suggesting the parallel secretory
mechanisms for release of pGluAbeta with Abeta40 and Abeta42, as well as with
neurotransmitter molecules, from large dense core vesicles. These results demonstrate that
pGluAbeta peptide is generated under normal conditions with Abeta40 and Abeta42 in the
regulated secretory pathway, which may provide a mechanism for their deposition in amyloid
plaques of Alzheimer‟s disease.
Disclosures: V.Y. Hook , American Life Science Pharmaceuticals, Inc., B. Research Grant
(principal investigator, collaborator or consultant and pending grants as well as grants already
received); American Life Science Pharmaceuticals, Inc., E. Ownership Interest (stock, stock
options, patent or other intellectual property); T. Toneff, None; G. Hook, American Life Science
Pharmaceuticals, Inc. (ALSP), A. Employment (full or part-time); ALSP, B. Research Grant
(principal investigator, collaborator or consultant and pending grants as well as grants already
received); ALSP, E. Ownership Interest (stock, stock options, patent or other intellectual
property).
Poster
243. Abeta Assembly and Deposition
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 243.7/K1
Topic: C.01.b. Abeta assembly and deposition
Support: Alzheimer‟s Association
The Mitchell Foundation
Title: Characterization of conformation and localization of different Aβ species of Alzheimer‟s
mouse models
Authors: *C. A. LASAGNA-REEVES, C. SOTO, R. KAYED;
Dept Neurol, Univ. Texas Med. Br., Galveston, TX
Abstract: Alzheimer‟s disease (AD) is a devastating neurodegenerative disorder and is one of
several disorders collectively known as the amyloid diseases. Other amyloid diseases include
Parkinson‟s disease (PD), Huntington disease (HD), type II diabetes, and the prion diseases. All
of these disorders are characterized by the deposition of proteinaceous aggregates, extracellular