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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
