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International Journal of Alzheimer’s Disease
Volume 2012 (2012), Article ID 376138, 17 pages
Research Article

Vaccine Development to Treat Alzheimer’s Disease Neuropathology in APP/PS1 Transgenic Mice

1Department of Neurosciences, EuroEspes Biotechnology, Polígono de Bergondo, Nave F, 15165 A Coruña, Spain
2EuroEspes Biomedical Research Center, Institute for CNS Disorders and Genomic Medicine and EuroEspes Foundation, 15166 La Coruña, Spain
3Neuroscience Division, Atlas Pharmaceuticals, Sunnyvale, CA 94089, USA

Received 15 May 2012; Revised 14 June 2012; Accepted 28 June 2012

Academic Editor: Francesco Panza

Copyright © 2012 Iván Carrera et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


A novel vaccine addressing the major hallmarks of Alzheimer’s disease (AD), senile plaque-like deposits of amyloid beta-protein (Aβ), neurofibrillary tangle-like structures, and glial proinflammatory cytokines, has been developed. The present vaccine takes a new approach to circumvent failures of previous ones tested in mice and humans, including the Elan-Wyeth vaccine (AN1792), which caused massive T-cell activation, resulting in a meningoencephalitis-like reaction. The EB101 vaccine consists of A đť›˝ 1 - 4 2 delivered in a novel immunogen-adjuvant composed of liposomes-containing sphingosine-1-phosphate (S1P). EB101 was administered to APPswe/PS1dE9 transgenic mice before and after AD-like pathological symptoms were detectable. Treatment with EB101 results in a marked reduction of Aβ plaque burden, decrease of neurofibrillary tangle-like structure density, and attenuation of astrocytosis. In this transgenic mouse model, EB101 reduces the basal immunological interaction between the T cells and immune activation markers in the affected hippocampal/cortical areas, consistent with decreased amyloidosis-induced inflammation. Therefore, immunization with EB101 prevents and reverses AD-like neuropathology in a significant manner by halting disease progression without developing behavioral spatial deficits in transgenic mice.