Neuroinflammatory Responses
Although neuroinflammation may have initial protective effects, chronic neuroinflammation may promote prolonged neurodegeneration such as that seen in PD, possibly via increased oxidative stress (Whitton, 2007). Whether neuroinflammation typically acts as an initial trigger of PD pathogenesis or is a downstream result of another triggering pathogenic event is unclear. Evidence for neuroinflammatory responses in PD includes the presence of activated microglia, increased expression of pro-inflammatory cytokines (TNF-alpha, IL-1-beta) and pro-inflammatory signaling cascades (NF-kappaB, COX-2). Furthermore, epidemiological data supports a reduce risk of PD in users of anti-inflammatory drugs (NSAIDS).
Reference:
Whitton PS. Inflammation as a causative factor in the aetiology of Parkinson's disease. Br J Pharmacol. 2007;150(8):963-76.
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04 Mar 2010
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