Neuroinflammation: A potential therapeutic target

Jeffrey M. Craft, D. Martin Watterson, Linda J. Van Eldik

Research output: Contribution to journalReview articlepeer-review

99 Scopus citations


The increased appreciation of the importance of glial cell-propagated inflammation (termed 'neuroinflammation') in the progression of pathophysiology for diverse neurodegenerative diseases, has heightened interest in the rapid discovery of neuroinflammation-targeted therapeutics. Efforts include searches among existing drugs approved for other uses, as well as development of novel synthetic compounds that selectively downregulate neuroinflammatory responses. The use of existing drugs to target neuroinflammation has largely met with failure due to lack of efficacy or untoward side effects. However, the de novo development of new classes of therapeutics based on targeting selective aspects of glia activation pathways and glia-mediated pathophysiologies, versus targeting pathways of quantitative importance in non-CNS inflammatory responses, is yielding promising results in preclinical animal models. The authors briefly review selected clinical and preclinical data that reflect the prevailing approaches targeting neuroinflammation as a pathophysiological process contributing to onset or progression of neurodegenerative diseases. The authors conclude with opinions based on recent experimental proofs of concept using preclinical animal models of pathophysiology. The focus is on Alzheimer's disease, but the concepts are transferrable to other neurodegenerative disorders with an inflammatory component.

Original languageEnglish
Pages (from-to)887-900
Number of pages14
JournalExpert Opinion on Therapeutic Targets
Issue number5
StatePublished - Oct 2005

Bibliographical note

Funding Information:
The research in the authors’ laboratories is supported by funds from the Institute for the Study of Aging and from NIH grants R37 AG13939, R01 AG20243, P01 AG21184, and R01 NS47586. JM Craft is a predoctoral scholar whose research has been supported by NIH training grant T32 AG00260, an NIH predoctoral fellowship F30 NS46942, and a predoctoral fellowship from the PhRMA Foundation.


  • Alzheimer's disease (AD)
  • Drug discovery
  • Multiple sclerosis
  • Natural product
  • Neuroinflammation
  • Nonsteroid anti-inflammatory drug (NSAID)
  • Parkinson's disease (PD)
  • Peroxisome proliferator-activated receptor γ (PPARγ)
  • Pyridazine

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology
  • Drug Discovery
  • Clinical Biochemistry


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