Int J Biol Sci 2019; 15(2):453-463. doi:10.7150/ijbs.26703 This issue

Research Paper

Changes in Chemokines and Chemokine Receptors Expression in a Mouse Model of Alzheimer's Disease

Adrián Jorda1, Omar Cauli2, Jose M. Santonja3, Martin Aldasoro1, Constanza Aldasoro1, Elena Obrador1, Jose Ma Vila1, Ma Dolores Mauricio1, Antonio Iradi1, Sol Guerra-Ojeda1, Patricia Marchio1, Soraya L. Valles1✉

1. Department of Physiology, School of Medicine, University of Valencia. Spain
2. Faculty of Surgery and Chiropody, University of Valencia. Spain
3. Clinic Hospital of Valencia. Spain

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Jorda A, Cauli O, Santonja JM, Aldasoro M, Aldasoro C, Obrador E, Vila JM, Mauricio MD, Iradi A, Guerra-Ojeda S, Marchio P, Valles SL. Changes in Chemokines and Chemokine Receptors Expression in a Mouse Model of Alzheimer's Disease. Int J Biol Sci 2019; 15(2):453-463. doi:10.7150/ijbs.26703. Available from

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Graphic abstract

The amyloid precursor protein plus presenilin-1 (APP/PS1) mice are a frequently-used model for Alzheimer's disease studies (AD). However, the data relevant to which proteins are involved in inflammatory mechanism are not sufficiently well-studied using the AD mouse model. Using behavioral studies, quantitative RT-PCR and Western-blot techniques, significant findings were determined by the expression of proteins involved in inflammation comparing APP/PS1 and Wild type mice. Increased GFAP expression could be associated with the elevation in number of reactive astrocytes. IL-3 is involved in inflammation and ABDF1 intervenes normally in the transport across cell membranes and both were found up-regulated in APP/PS1 mice compared to Wild type mice. Furthermore, CCR5 expression was decreased and both CCL3 and CCL4 chemokines were highly expressed indicating a possible gliosis and probably an increase in chemotaxis from lymphocytes and T cell generation. We also noted for the first time, a CCR8 increase expression with diminution of its CCL1 chemokine, both normally involved in protection from bacterial infection and demyelination. Control of inflammatory proteins will be the next step in understanding the progression of AD and also in determining the mechanisms that can develop in this disease.

Keywords: Alzheimer's disease, chemokine receptors, chemotaxis, inflammation, behavior