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BioMed Research International
Volume 2013 (2013), Article ID 709145, 12 pages
Research Article

Immunocytochemical Characterization of Alzheimer Disease Hallmarks in APP/PS1 Transgenic Mice Treated with a New Anti-Amyloid-β Vaccine

1Department of Neurosciences, EuroEspes Biotechnology, 15165 La Coruna, Spain
2Department of Human Sciences, Texas A&M University-Kingsville, Kingsville, TX, USA
3Atlas Pharmaceuticals, Sunnyvale, CA, USA
4National Institute on Aging, National Institutes of Health, Baltimore, MD, USA
5Medical Center of the Administration of the President of the Republic of Kazakhstan, Astana, Kazakhstan
6EuroEspes Biomedical Research Center, Institute for CNS Disorders and Genomic Medicine, 15165 La Coruna, Spain
7“GALLY” International Biomedical Research Consulting LLC, San Antonio, TX, USA
8Department of Health Science and Healthcare Administration, University of Atlanta, Atlanta, GA, USA

Received 10 April 2013; Revised 11 June 2013; Accepted 2 July 2013

Academic Editor: Aaron Dumont

Copyright © 2013 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.


APP/PS1 double-transgenic mouse models of Alzheimer’s disease (AD), which overexpress mutated forms of the gene for human amyloid precursor protein (APP) and presenilin 1 (PS1), have provided robust neuropathological hallmarks of AD-like pattern at early ages. This study characterizes immunocytochemical patterns of AD mouse brain as a model for human AD treated with the EB101 vaccine. In this novel vaccine, a new approach has been taken to circumvent past failures by judiciously selecting an adjuvant consisting of a physiological matrix embedded in liposomes, composed of naturally occurring phospholipids (phosphatidylcholine, phosphatidylglycerol, and cholesterol). Our findings showed that administration of amyloid-β1−42 (Aβ) and sphingosine-1-phosphate emulsified in liposome complex (EB101) to APP/PS1 mice before onset of Aβ deposition (7 weeks of age) and/or at an older age (35 weeks of age) is effective in halting the progression and clearing the AD-like neuropathological hallmarks. Passive immunization with EB101 did not activate inflammatory responses from the immune system and astrocytes. Consistent with a decreased inflammatory background, the basal immunological interaction between the T cells and the affected areas (hippocampus) in the brain of treated mice was notably reduced. These results demonstrate that immunization with EB101 vaccine prevents and attenuates AD neuropathology in this type of double-transgenic mice.