Is a breakdown of the blood-brain barrier cause or effect?

Stanley H. Appel, James L. McManaman

Research output: Contribution to journalArticlepeer-review

1 Scopus citations


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 raphé 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.

Original languageEnglish (US)
Pages (from-to)512-514
Number of pages3
JournalNeurobiology of Aging
Issue number6
StatePublished - 1986

ASJC Scopus subject areas

  • Neuroscience(all)
  • Aging
  • Clinical Neurology
  • Developmental Biology
  • Geriatrics and Gerontology


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