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1 Acta Neurobiologiae Experimentalis

1 2017

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The effect of alpha-synuclein on initiation of inflammatory reaction in the murine brain

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Joniec-Maciejak I. , Wawer A. , Sznejder-Pachołek A. , Wojnar E. , Mirowska-Guzel D.

nr Suppl.1

INTRODUCTION: Parkinson’s disease (PD), one of the most common neurological disorder, is characterized by the loss of dopaminergic neurons in substantia nigra and striatum (ST). The typical reaction of central nervous system (CNS) on neurodegenerative processes is microglia activation and the inflammatory reaction. The data suggests that increased level of α‑synuclein (ASN), a small protein which is the major component of Lewy bodies, can induce microglia activation. Activated microglial cells release proinflammatory and potentially cytotoxic substances like cytokines. Till now, little is known about in vivo effects of exogenous ASN monomers on initiation of neuroinflammation and neurodegeneration. AIM(S): The aim of the present study was to examine the effect of increased ASN monomers concentration on microglia response and expression of pro‑ and anti‑inflammatory cytokines (interleukin 1α (IL‑1α), IL‑10, IL‑12) in the ST. METHOD(S): Male and female C57Bl/10 Tar mice 9 month-old were used in this study. Human recombinant ASN was bilaterally administered into ST (single treatment – 4 μg / structure, 8 μg per brain) and mice were decapitated after 4 or 12 weeks post injection. The changes in the level of inflammatory factors in ST were evaluated using Real-Time PCR and enzyme-linked immunosorbent assay (ELISA). RESULTS: We observed increased level of a microglia marker – ionized calcium-binding adapter molecule 1 (IBA1) protein after ASN injection into ST. We noticed also some differences in the level of one of the most important pro inflammatory cytokines – IL‑1α. CONCLUSIONS: Our study showed that monomers of ASN are strongly involved in the inflammatory reaction in the murine CNS. Further studies are required to reveal the detailed mechanism of the influence of ASN on neuroinflammation in course of Parkinson’s disease. FINANCIAL SUPPORT: This study was supported by Grant No 1M9/PM 2/16 (Medical University of Warsaw). Research subject was implemented with CePT infrastructure financed by the European Union – The Europan Regional Development Fund within the operational programme “Innovative economy for 2007–2013.