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. 2012 Aug 5;2012:345472. doi: 10.1155/2012/345472

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Copyright © 2012 Nicole M. Desforges et al.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Initiation of inflammatory response following intraneuronal protein accumulation. Intraneuronal accumulation of pathogenic proteins causes ATP release by apoptotic neurons to activate purinergic microglia P2X7 receptors or TLRs. Activated microglia release proinflammatory cytokines (TNF-α, IL-16, IL-1) and iNOS to activate astrocytes (via MCP-1 chemotaxis) and increase apoptosis in stressed neurons. To initiate a neuroprotective immune response, injured neurons may communicate via fractalkine (CX3CR1) and suppress inflammation.