alexa Combinatorial Vaccine against Complement Factor C5a and Amyloid Beta: A New Therapeutic Approach in Alzheimers Disease
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
Open Access

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Research Article

Combinatorial Vaccine against Complement Factor C5a and Amyloid Beta: A New Therapeutic Approach in Alzheimers Disease

Landlinger C1*, Mihailovska E1, Mandler M2, Galabova G1 and Staffler G1*

1AFFiRiS AG, Karl-Farkas-Gasse 22, 1030 Vienna 1030, Austria

2Accanis Biotech F&E GmbH & C0 KG, Karl-Farkas-Gasse 22, 1030 Vienna, Austria

*Corresponding Authors:
Christine Landlinger
PhD, AFFiRiS AG, Karl-Farkas-Gasse 22
Vienna, 1030, Austria
Tel: +43-17981575-367
Fax: +43-17981575-311
E-mail: [email protected]
 
Guenther Staffler
PhD, AFFiRiS AG, Karl-Farkas-Gasse 22
Vienna, 1030, Austria
Tel: +43-17981575-321
Fax: +43-17981575-311
E-mail: [email protected]

Received date: December 15, 2016; Accepted date: January 25, 2017; Published date: January 31, 2017

Citation: Landlinger C, Mihailovska E, Mandler M, Galabova G, Staffler G (2017) Combinatorial Vaccine against Complement Factor C5a and Amyloid Beta: A New Therapeutic Approach in Alzheimer’s Disease. J Clin Cell Immunol 8:487. doi: 10.4172/2155-9899.1000487

Copyright: © 2017 Landlinger C, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Alzheimer’s disease (AD) is the most common neurodegenerative disease characterized by neuronal loss due to amyloid beta (Aβ) aggregations, neurofibrillary tangles, and prominent neuroinflammation. Inflammatory processes in AD primarily occur in response to misfolded and aggregated proteins, or mislocalized nucleic acids and reactive microglia. Prolonged chronic neuroinflammation is thought to reinforce neuronal cell dysfunction and cell death. In our previous study we demonstrated that the interference with the pro-inflammatory mediator C5a by AFF1 vaccine at an early stage of disease is able to reduce microglia activation and amyloid plaque burden which is accompanied by ameliorated memory deficiency in Tg2576 mice, a mouse model of AD. In a follow-up study we tested the effect of a combinatorial vaccine targeting neuroinflammation by C5a and Aβ aggregates, two detrimental processes in AD. The amyloid plaque burden in the brain of Tg2576 mice was significantly reduced upon vaccination by the monovalent anti-C5a (AFF1) as well as anti-Aβ (AD02) vaccine, however, the combinatorial AFF1/AD02 vaccine showed a clear additive beneficial effect. Moreover, contextual memory in Tg2576 mice was significantly improved by the combinatorial AFF1/AD02 vaccine when compared to monovalent or control vaccines. Thus, targeting two neuropathological processes such as neuroinflammation and Aβ aggregation may represent a new and promising approach for the treatment of AD.

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