Our data suggest that the transfer of AAV2-hIL-10 into the striatum may play a neuroprotective role in the mouse MPTP model of PD and these effects are mediated by the anti-inflammatory action of IL-10.

Our results suggest that both the microglia activation and supressing astrocytes play a crucial role in ASN-related dopaminergic neurotoxicity.

The results revealed protective properties of AAV2-hIL-10.

Alpha-synuclein (ASN) is a small presynaptic protein which is the major component of Lewy bodies-the histological hallmark of Parkinson's disease. Among many functions, ASN plays an important role in regulation of dopaminergic system by controlling dopamine concentration at nerve terminals. An abnormal structure or excessive accumulation of ASN in the brain can induce neurotoxicity leading to the dopaminergic neurodegeneration. To date, several transgenic mouse lines overexpressing ASN have been generated and there are several studies using injections of ASN fibrils into the murine brain. However, still is little known about the effects of exogenously applied ASN monomers on dopaminergic neurotransmission. In this study we investigated the influence of cerebral injection of human ASN on dopaminergic system activity. We have demonstrated that a single injection of ASN monomers into the substantia nigra pars compacta or striatum is sufficient to affect dopaminergic neurotransmission in murine nigro-striatal system.

No abstract