Non steroidal anti-inflammatory drugs (NSAIDs) are therapeutic agents of first choice for the treatment of inflammation, pain, and fever. Neuroscience research of the last decades has pointed out the important role of inflammation in the pathogenesis of several brain disorders, and epidemiological and experimental evidence has suggested a beneficial role of NSAIDs in both chronic and acute neuropathologies. More recently NSAIDs have gained further attention as potential tools to enhance neuroregenerative processes in the adult mammalian brain. The rational behind their use arises from the notion that inflammatory processes that accompany brain damage would exert a major detrimental effect on endogenous neurogenesis. However, inflammation and glial responses to acute or chronic injuries constitute a complex and multifaceted process by which, besides potentially harmful and cytotoxic activities, beneficial responses can be initiated in the attempt to re-establish the lost tissue integrity. The individuation of optimal timing and type of pharmacological intervention able to potentiate the beneficial aspects of inflammation rather than to suppress it as a whole, would allow the achievement of enhanced and successful regenerative responses. In the present article, we will review the current literature on the effects of NSAIDs on neurogenesis and briefly discuss the cellular or molecular mechanisms by which these drugs can modulate brain restorative processes.
Keywords: NSAID, neurogenesis, cyclooxygenase (COX), neural stem progenitor cells, inflammation
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