Abstract
Amyloid deposits resembling plaques found in Alzheimer's disease (AD) brains were formed in the brains of non-transgenic BALB/c mice following intranasal infection with Chlamydia pneumoniae. The mice were infected at 3 months of age with C. pneumoniae isolated from an AD brain. Infection was confirmed by light and electron microscopy in olfactory tissues of the mice. C. pneumoniae was still evident in these tissues 3 months after the initial infection indicating that a persistent infection had been established. Amyloid beta (Aß) 1-42 immunoreactive deposits were identified in the brains of infected BALB/c mice up to 3 months post-infection with the density, size, and number of deposits increasing as the infection progressed. A subset of deposits exhibited thioflavin-s labeling. Intracellular Aß1-42 labeling was observed in neuronal cells. Experimental induction of amyloid deposition in brains of non-transgenic BALB/c mice following infection with C. pneumoniae may be a useful model for furthering our understanding of mechanisms, linked to infection, involved in the initiation of the pathogenesis of sporadic AD.
Original language | American English |
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Journal | Neurobiology of aging |
Volume | 25 |
State | Published - Jan 1 2004 |
Keywords
- Alzheimer disease
- Alzheimer's disease
- Amyloid
- Amyloid beta-Protein
- Animal model
- Animals
- Bacteria
- Brain
- Cell Line
- Chlamydophila (Chlamydia) pneumoniae
- Chlamydophila Infections
- Chlamydophila pneumoniae
- Humans
- Inbred BALB C
- Infection
- Mice
- Mouse
- Non-transgenic
- Olfactory
- Peptide Fragments
- Plaque
- Senile Plaques
- Sporadic AD
- article
- bacterial infection
- bacterium isolation
- controlled study
- density
- disease course
- electron microscopy
- female
- immunoreactivity
- mouse strain
- nonhuman
- olfactory tract
- pathogenesis
- priority journal
- rat
- thioflavine
Disciplines
- Molecular and Cellular Neuroscience