Microglia as a potential bridge between the amyloid β-peptide and tau

Masashi Kitazawa, Tritia R. Yamasaki, Frank M. LaFerla

Research output: Contribution to journalArticlepeer-review

150 Scopus citations

Abstract

Inflammation is a critical component of the pathogenesis of Alzheimer's disease (AD), consisting of the activation of both microglia and astrocytes. Activated microglia and reactive astrocytes are found in and around extraneuronal amyloid-β plaques and are thought to facilitate the clearance of these deposits from the brain parenchyma. However, mounting evidence indicates that chronic activation of microglia, presumably via the secretion of cytokines and reactive molecules, may exacerbate plaque pathology as well as enhance the hyperphosphorylation of tau and the subsequent development of neuroflbrillary tangles. Thus, suppression of microglial activity in AD brain has been considered as a potential treatment of AD and may slow the disease progression. Along these lines, anti-inflammatory drugs, particularly non-steroidal anti-inflammatory drugs (NSAIDs), lessen the effects of AD pathology. In this review, we discuss the molecular mechanism of inflammatory responses in AD brain as well as animal models, and current therapies using NSAIDs, antioxidants, and immunotherapy as neuroprotective strategies for AD.

Original languageEnglish
Pages (from-to)85-103
Number of pages19
JournalAnnals of the New York Academy of Sciences
Volume1035
DOIs
StatePublished - 2004

Keywords

  • Antioxidant
  • Immunotherapy
  • Interleukins
  • NSAID
  • p38-MAPK

ASJC Scopus subject areas

  • General Neuroscience
  • General Biochemistry, Genetics and Molecular Biology
  • History and Philosophy of Science

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