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. 2010 Mar;8(1):62-8.
doi: 10.2174/157015910790909485.

Cyclooxygenase and neuroinflammation in Parkinson's disease neurodegeneration

Anna L Bartels  1 , Klaus L Leenders
Affiliations

Cyclooxygenase and neuroinflammation in Parkinson's disease neurodegeneration

Anna L Bartels et al. Curr Neuropharmacol. 2010 Mar.

Abstract

Cyclooxygenase (COX) expression in the brain is associated with pro-inflammatory activities, which are instrumental in neurodegenerative processes such as Parkinson's disease (PD). It is discussed that drugs with the capacity to rescue dopaminergic neurons from microglia toxicity and neuroinflammatory processes may result in an amelioration of parkinsonian symptoms by delaying the onset or slowing progression. This article reviews the involvement of COX in neuroinflammation, specifically focussing at the role of selective COX-2 inhibition in neuroinflammation and neurodegeneration in Parkinson's disease.

Keywords: COX-2; Parkinson; microglia; neurodegeneration; neuroinflammation; neuroprotection..

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Figures

Fig. (1)
Fig. (1)
Microglia and COX involvement in neuronal injury. Various stimuli can activate microglia in Parkinson’s disease, including aggregated α-synuclein, toxins (such as MPTP, 6-OHDA, LPS, rotenone, paraquat, pesticides). Intracellular signalling cascades involving NF-κB and MAP kinases lead to microglial activation and induction of proinflammatory mediators, including iNOS, NADPH oxidase and COX-2, and the subsequent release of cytokines (e.g. IL-1β, IL-6, TNF-α), nitric oxide (NO) and prostaglandins (including PGE2). COX-1 is constitutively expressed on microglia and may be the primary source of PGE2 release in early inflammation phases. COX-2 is localized in neurons and contributes to PGE synthesis in response to neuronal insults. Astrocyte activation may increase glutamate levels with cytokine and COX-2 induction.
See this image and copyright information in PMC

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