Is a breakdown of the blood-brain barrier cause or effect? Academic Article uri icon


MeSH Major

  • Amyotrophic Lateral Sclerosis
  • Immunotherapy
  • Neuroimmunomodulation
  • Parkinson Disease
  • T-Lymphocytes, Regulatory


  • Several alternative explanations for the pathogenesis of Alzheimer's disease proposed by Hardy et al. are presented. From our vantage point, the amyloid deposition and alterations in the blood-brain barrier in Alzheimer's disease are less likely related to impaired projections of locus ceruleus, nucleus basalis, and raph√© nucleus than to a primary insult to the blood vessels produced by a humoral or cell-mediated immune attack. Such an attack would then be associated with the formation of neuritic plaques which increasingly engulf pre-synaptic and post-synaptic neuronal constituents as well as surrounding glia. Such a process could then interrupt the retrograde trophic effects of post-synaptic cortical cells upon projecting subcortical cells, resulting in degeneration of the projecting cells and impairment of cognitive function characteristic of Alzheimer's disease. ¬© 1986.

publication date

  • January 1986



  • Academic Article


Digital Object Identifier (DOI)

  • 10.1016/0197-4580(86)90094-1

Additional Document Info

start page

  • 512

end page

  • 514


  • 7


  • 6