Abstract
There is increasing evidence that neuroinflammation drives the progression of neurodegenerative disease. We are accumulating evidence that excessive complement activation in the brain leading to C5a generation, contributes to neuronal cell death in rodent models of neurodegenerative disease. The current study explored the expression of complement in two mouse models of neurodegenerative disease. Our findings demonstrate that complement activation, C5a generation, and C5a receptor upregulation are key events in these neurodegenerative models. Reducing complement-induced neuroinflammation could be an important therapeutic strategy to treat a wide variety of neurodegenerative diseases.
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