Abstract:
:The characteristic insoluble, senile (neuritic) plaques found extracellularly in brains of patients with Alzheimer's disease (AD) contain the fibrillar form of beta-amyloid (Abeta42). A substantial proportion of autopsied elderly brains have demonstrated DNA evidence of herpes simplex virus type 1 (HSV-1) infiltration. HSV-1-infected cells produce significant quantities of non-infectious, non-DNA-containing light particles (L-particles) comprised of viral envelope and tegument proteins. HSV-induced L-particles can be exocytosed out of their host cells. This report advances the hypothesis that (1) Abeta binds to L-particles; (2) Abeta permeabilizes L-particles, destroying the integrity of the envelope and allowing the contained tegument proteins to spill into the extracellular space; and (3) these events are followed by a conformational shift of Abeta into its fibrillar form, physically trapping the L-particle-derived substances and resulting in the plaques characteristic of AD. These hypotheses are supported by reports of biomolecular changes and pathophysiologies which have been simultaneously observed in both AD- and HSV-infected brains.
journal_name
Med Hypothesesjournal_title
Medical hypothesesauthors
Kammerman EM,Neumann DM,Ball MJ,Lukiw W,Hill JMdoi
10.1016/j.mehy.2005.07.033keywords:
subject
Has Abstractpub_date
2006-01-01 00:00:00pages
294-9issue
2eissn
0306-9877issn
1532-2777pii
S0306-9877(05)00421-4journal_volume
66pub_type
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pub_type: 信件
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pub_type: 杂志文章,评审
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