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


 

 

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Immunocytochemical 

Characterization of Alzheimer’s 

Disease Hallmarks in APP/PS1 

Transgenic Mice Treated with a 

New Anti-Amyloid-𝛽 Vaccine 
 

Ivan Carrera1, Ignacio 

Etcheverria1, Yi Li2, Lucia 

Fernandez-Novoa1, Valter 

Lombardi1, Carmen Vigo3, Hector 

H. Palacios4, Valery V. Benberin5, 

Ramon Cacabelos6, Gjumrakch 

Aliev7,8 
 

1Department of Neurosciences, 
EuroEspes Biotechnology, La Coruna, 
Spain; 2Yale University School of 
Medicine, New Haven, CT; 3Atlas 
Pharmaceuticals, Sunnyvale, CA; 
4National Institute on Aging, National 
Institutes of Health, Baltimore, MD; 
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, La Coruna, Spain; 7GALLY 
International Biomedical Research 
Consulting LLC, San Antonio, TX; 
8Department of Health Science and 
Healthcare Administration, University of 
Atlanta, Atlanta, GA 

 

Vol. 2, Suppl. (2013)   |   ISSN 2166-7403 (online)     

DOI 10.5195/cajgh.2013.119   |   http://cajgh.pitt.edu 

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CARRERA 

 

 

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Central Asian Journal of Global Health 

Volume 2, Suppl. (2013)  |  ISSN 2166-7403 (online) |  DOI 10.5195/cajgh.2013.119 |  http://cajgh.pitt.edu 

  

 

Abstract 

Introduction: APP/PS1 double-transgenic mouse models of Alzheimer’s disease (AD), which overexpress mutated forms of the 

gene for the human amyloid precursor protein (APP) and presenilin 1 (PS1), have provided robust neuropathological hallmarks of 

an AD-like pattern at early ages. This study aimed to characterize immunocytochemical patterns of the AD mouse brain, which is 

treated with the EB101 vaccine, as a model for human AD.  

 

Material and methods: In this novel vaccine, a new approach has been taken to circumvent past failures with A𝛽 vaccines by 

judiciously selecting an adjuvant consisting of a physiological matrix embedded in liposomes, composed of naturally occurring 

phospholipids (phosphatidylcholine, phosphatidylglycerol, and cholesterol). 

 

Results: Our findings showed that the administration of amyloid-𝛽1−42 (A𝛽) and sphingosine-1-phosphate emulsified in 

liposome complex (EB101) to APP/PS1 mice before the onset of A𝛽 brain deposition (at 7 weeks of age) and/or at an older age 

(35 weeks of age) can be effective in both halting the progression and clearing the AD-like neuropathological hallmarks. In 

addition, 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. 

 

Conclusion: These results provide strong evidence that immunization with the EB101 vaccine prevents and attenuates AD 

neuropathology in this type of double-transgenic mice.  

Keywords: Alzheimer’s disease, anti-amyloid-𝛽 vaccine 

 

 

 

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