Inflammatory mechanisms in Alzheimer's disease: implications for therapy

Am J Psychiatry. 1994 Aug;151(8):1105-13. doi: 10.1176/ajp.151.8.1105.


Objective: The purpose of this article is to review evidence that inflammatory and immune mechanisms are important in the pathophysiology of Alzheimer's disease and to suggest new treatment strategies.

Method: The authors review the English-language literature of the last 10 years pertaining to the pathophysiology of Alzheimer's disease.

Results: There is ample evidence supporting the hypothesis that inflammatory and immune mechanisms are involved in tissue destruction in Alzheimer's disease. Acute phase proteins are elevated in the serum and are deposited in amyloid plaques, activated microglial cells that stain for inflammatory cytokines accumulate around senile plaques, and complement components including the membrane attack complex are present around dystrophic neurites and neurofibrillary tangles.

Conclusions: Clinical trials of anti-inflammatory/immunosuppressive drugs are necessary to determine whether alteration of these inflammatory mechanisms can slow the progression of Alzheimer's disease.

Publication types

  • Review

MeSH terms

  • Acute-Phase Proteins / immunology
  • Acute-Phase Proteins / physiology
  • Acute-Phase Reaction / immunology
  • Acute-Phase Reaction / physiopathology
  • Alzheimer Disease / drug therapy
  • Alzheimer Disease / etiology
  • Alzheimer Disease / physiopathology*
  • Anti-Inflammatory Agents / therapeutic use
  • Brain / immunology
  • Brain / physiopathology
  • Complement Membrane Attack Complex / immunology
  • Cytokines / physiology
  • Encephalitis / immunology
  • Encephalitis / physiopathology
  • Humans
  • Immune System / physiopathology
  • Immunosuppressive Agents / therapeutic use
  • Inflammation / complications
  • Inflammation / drug therapy
  • Inflammation / physiopathology*
  • Neurofibrillary Tangles / immunology


  • Acute-Phase Proteins
  • Anti-Inflammatory Agents
  • Complement Membrane Attack Complex
  • Cytokines
  • Immunosuppressive Agents