Abstract
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 language | English (US) |
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Pages (from-to) | 512-514 |
Number of pages | 3 |
Journal | Neurobiology of Aging |
Volume | 7 |
Issue number | 6 |
DOIs | |
State | Published - 1986 |
ASJC Scopus subject areas
- General Neuroscience
- Aging
- Clinical Neurology
- Developmental Biology
- Geriatrics and Gerontology