Involvement of inflammation in Alzheimer's disease pathogenesis and therapeutic potential of anti-inflammatory agents

Sina Shadfar, Chul Ju Hwang, Mi-Sun Lim, Dong-Young Choi, Jin Tae Hong

Research output: Contribution to journalReview articlepeer-review

112 Citations (Scopus)


Alzheimer's disease (AD) is the most common form of dementia. It is characterized by beta-amyloid (Aβ) peptide fibrils, which are extracellular depositions of a specific protein, and is accompanied by extensive neuroinflammation. Various studies have demonstrated risk factors that can affect AD pathogenesis, and they include accumulation of Aβ, hyperphosphorylation of tau protein, and neuroinflammation. Among these detrimental factors, neuroinflammation has been highlighted by epidemiologic studies suggesting that use of anti-inflammatory drugs could significantly reduce the incidence of AD. Evidence suggests that astrocytes, microglia, and infiltrating immune cells from periphery might contribute to or modify the process of neuroinflammation and neurodegeneration in AD brains. In addition, recent data indicate that microRNAs may affect neuroinflammatory responses in the brain. This article focuses on supportive evidence that neuroinflammation plays a critical role in AD development. In addition, we depict putative therapeutic capacity of anti-inflammatory drugs for AD prevention or treatment. We also discuss pathogenic mechanisms by which astrocytes, microglia, T cells and microRNA participate in AD and the neuroprotective mechanisms of anti-inflammatory drugs.

Original languageEnglish
Pages (from-to)2106-19
Number of pages14
JournalArchives of Pharmacal Research
Issue number12
Publication statusPublished - Dec 2015
Externally publishedYes


  • Alzheimer’s disease
  • Amyloidogenesis
  • Anti-inflammatory
  • Beta-amyloid
  • Neuroinflammation
  • Alzheimer's disease


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