Abstract:

There is ample and increasing evidence, from studies of human pathology, animal models and tissue culture, that chronic inflammation occurs in the basal ganglia in patients with Parkinson's disease. In such inflammatory states, activated glia can produce large quantities of free radicals and other neurotoxic materials. Dopaminergic neurons appear to be particularly vulnerable to these neurotoxins.

The anti-inflammatory drugs that are presently in wide use act on peripheral players in the inflammatory process. Many experiments are under way to find agents that inhibit more potent contributors, such as the activated microglia or terminal complement proteins. Whether such drugs will slow the process of Parkinson's disease or reduce the high risk of dementia in such patients remains to be determined in future work.

Keywords: Anti inflammatories; Inflammation; Nonsteroidal anti inflammatories; Parkinson's disease

Document Type: Leading article

Affiliations: 1: Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, British Columbia, Canada