Inflammation and Alzheimer's disease

Arch Pharm Res. 2010 Oct;33(10):1539-56. doi: 10.1007/s12272-010-1006-7. Epub 2010 Oct 30.


Alzheimer's disease (AD) is the most common form of dementia. It is characterized by extracellular deposition of a specific protein, beta-amyloid peptide fibrils, and is accompanied by extensive loss of neurons in the brains of affected individuals. Although the pathophysiologic mechanism is not fully established, inflammation appears to be involved. Neuroinflammation has been known to play a critical role in the pathogenesis of chronic neurodegenerative disease in general, and in AD in particular. Numerous studies show the presence of a number of markers of inflammation in the AD brain: elevated inflammatory cytokines and chemokines, and accumulation of activated microglia in the damaged regions. Epidemiological studies have shown that long-term use of non-steroidal anti-inflammatory drugs suppresses the progression of AD and delays its onset, suggesting that there is a close correlation between neuroinflammation and AD pathogenesis. The aim of this review is (1) to assess the association between neuroinflammation and AD through discussion of a variety of experimental and clinical studies on AD and (2) to review treatment strategies designed to treat or prevent AD.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Alzheimer Disease / drug therapy
  • Alzheimer Disease / physiopathology*
  • Alzheimer Disease / prevention & control
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • Astrocytes / metabolism
  • Brain / metabolism
  • Brain / pathology
  • Encephalitis / drug therapy
  • Encephalitis / etiology*
  • Humans
  • Inflammation Mediators / metabolism
  • Microglia / metabolism
  • Neuritis / drug therapy
  • Neuritis / etiology*
  • Neurons / metabolism
  • Oxidative Stress / drug effects
  • PPAR gamma / agonists


  • Anti-Inflammatory Agents, Non-Steroidal
  • Inflammation Mediators
  • PPAR gamma