The inflammatory cascade hypothesis

Reactive gliosis and microglial activation are consistent findings in AD brain with a host of inflammatory mediators (e.g., complement proteins, cytokines, and chemokines) being present at higher levels than in normal brain. These observations support an inflammatory hypothesis of AD that postulates that either neurodegeneration in AD brain is secondary to an inflammatory response to senile plaques and NFTs (cause) or inflammation triggers formation of NFTs and senile plaques, which in turn activate immune reactions that drive a cycle of neuronal destruction.20

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