Copyright 2003 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2003
CLINICALLY APPLICABLE and effective maneuvers to protect the nervous system from selective neurodegenerative diseases have been elusive. Although the etiology and pathogenesis of Alzheimer disease (AD), amyotrophic lateral sclerosis, and idiopathic Parkinson disease (PD) are distinctly different, they share common pathogenic mechanisms in the process of neuronal cell death and degeneration. There is substantial evidence of a role for glial cell–mediated inflammation in the neurodegenerative process responsible for AD, amyotrophic lateral sclerosis, and PD.1-3 This inflammatory response is an obvious target for potential therapeutic intervention. By far, the largest number of epidemiological studies and clinical trials analyzing the effects of modulators of inflammation (namely nonsteroidal anti-inflammatory drugs [NSAIDs],4 steroids, hormones, and aspirin) on disease risk,5 rate of progression, and cognitive function have been conducted on patients with AD. Despite the many studies, the outcomes have been inconsistent and inconclusive and have not permitted a consensus for any of these modulators as an effective or primary therapeutic intervention.4,5 The situation for PD may be developing more favorably. In this issue of the ARCHIVES, Chen et al6 report the first convincing epidemiological data for a therapeutic benefit from neuroimmune modulation, specifically regarding the beneficial effects of NSAIDs and aspirin on the risk of PD.
Schiess M. Nonsteroidal Anti-inflammatory Drugs Protect Against Parkinson NeurodegenerationCan an NSAID a Day Keep Parkinson Disease Away?. Arch Neurol. 2003;60(8):1043–1044. doi:10.1001/archneur.60.8.1043
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