Abstract
BackgroundSporadic late-onset Alzheimer's disease (AD) appears to evolve from an interplay between genetic and environmental factors. One environmental factor that continues to be of great interest is that of Chlamydia pneumoniae infection and its association with late-onset disease. Detection of this organism in clinical and autopsy samples has proved challenging using a variety of molecular and histological techniques. Our current investigation utilized immunohistochemistry with a battery of commercially available anti-C. pneumoniae antibodies to determine whether C. pneumoniae was present in areas typically associated with AD neuropathology from 5 AD and 5 non-AD control brains.ResultsImmunoreactivity for C. pneumoniae antigens was observed both intracellularly in neurons, neuroglia, endothelial cells, and peri-endothelial cells, and extracellularly in the frontal and temporal cortices of the AD brain with multiple C. pneumoniae-specific antibodies. This immunoreactivity was seen in regions of amyloid deposition as revealed by immunolabeling with two different anti-beta amyloid antibodies. Thioflavin S staining, overlaid with C. pneumoniae immunolabeling, demonstrated no direct co-localization of the organism and amyloid plaques. Further, the specificity of C. pneumoniae labeling of AD brain sections was demonstrated using C. pneumoniae antibodies pre-absorbed against amyloid β 1-40 and 1-42 peptides.ConclusionsAnti-C. pneumoniae antibodies, obtained commercially, identified both typical intracellular and atypical extracellular C. pneumoniae antigens in frontal and temporal cortices of the AD brain. C. pneumoniae, amyloid deposits, and neurofibrillary tangles were present in the same regions of the brain in apposition to one another. Although additional studies are required to conclusively characterize the nature of Chlamydial immunoreactivity in the AD brain, these results further implicate C. pneumoniae infection with the pathogenesis of Alzheimer's disease.
Highlights
Sporadic late-onset Alzheimer’s disease (AD) appears to evolve from an interplay between genetic and environmental factors
C. pneumoniae immunolabeling in AD tissue All available sections from the frontal and temporal cortices of AD and control brains were immunolabeled with anti-C. pneumoniae antibodies listed in table 1
An AD brain immunolabeled with no primary antibody and both an anti-mouse horseradish peroxidase (HRP) conjugated secondary and an anti-mouse alkaline phosphatase (AP) conjugated secondary reacted with both 3, 3′-Diaminobenzidine (DAB) and AP red illustrate the absence of non specific immunolabeling in the temporal cortex
Summary
Sporadic late-onset Alzheimer’s disease (AD) appears to evolve from an interplay between genetic and environmental factors. One environmental factor that continues to be of great interest is that of Chlamydia pneumoniae infection and its association with late-onset disease. Detection of this organism in clinical and autopsy samples has proved challenging using a variety of molecular and histological techniques. Distinctive pathological hallmarks associated with the disease include tau accumulations forming neuropil threads (NTs) and neurofibrillary tangles (NFTs), and deposits of extracellular amyloid comprising neuritic senile plaques (NSPs). There are two distinct forms of Alzheimer’s disease, familial AD and sporadic late-onset AD. The extracellular accumulations of amyloid in the brain are composed principally of amyloid b 1-40 and 1-42 and form neuritic senile plaques (NSP) [1,2]. Since late-onset AD lacks the same mutations seen in familial AD, determination of the cause of amyloid pathology in late-onset AD remains poorly understood
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