Insights into the neurodegenerative process of Alzheimer's disease: A role for mononuclear phagocyte-associated inflammation and neurotoxicity

Robin L. Cotter, William J. Burke, Vince S. Thomas, Jane F. Potter, Jialin Zheng, Howard E. Gendelman

Research output: Contribution to journalReview article

72 Scopus citations

Abstract

Since the first description of Alzheimer's disease (AD) in 1907, significant progress was made into understanding disease pathophysiology. The enormous effort in AD research has translated into the discovery of genetic linkages for disease, into elucidating the structure and function of the etiologic β-amyloid protein, and into unraveling the seemingly complex neuroimmunological cascade that affects neuronal dysfunction. Although effective therapies do not currently exist, many are being developed. We propose that the neuropathogenesis of AD, in measure, revolves around the immunological activation of glial cells, which in turn leads to alterations in inflammatory neurotoxin production, and ultimately to neuronal injury and death. Elucidating the mechanisms involved in such glial cell immune activation should provide valuable insights into understanding the disease process and in providing effective therapeutics to prevent and/or retard the devastating neurodegeneration that afflicts so many of our elderly.

Original languageEnglish (US)
Pages (from-to)416-427
Number of pages12
JournalJournal of Leukocyte Biology
Volume65
Issue number4
DOIs
StatePublished - 1999

Keywords

  • Apoptosis
  • Central nervous system
  • Complement
  • Immunopathology
  • Mononuclear phagocytes
  • Neurotrophins
  • Pro-inflammatory cytokines
  • Signal transduction
  • β- amyloid protein

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Cell Biology

Fingerprint Dive into the research topics of 'Insights into the neurodegenerative process of Alzheimer's disease: A role for mononuclear phagocyte-associated inflammation and neurotoxicity'. Together they form a unique fingerprint.

  • Cite this