IDENTIFICATION AND LOCALIZATION OF CHLAMYDIA-PNEUMONIAE IN THE ALZHEIMERS BRAIN

Citation
Bj. Balin et al., IDENTIFICATION AND LOCALIZATION OF CHLAMYDIA-PNEUMONIAE IN THE ALZHEIMERS BRAIN, Medical microbiology and immunology, 187(1), 1998, pp. 23-42
Citations number
97
Categorie Soggetti
Microbiology,Immunology
ISSN journal
03008584
Volume
187
Issue
1
Year of publication
1998
Pages
23 - 42
Database
ISI
SICI code
0300-8584(1998)187:1<23:IALOCI>2.0.ZU;2-G
Abstract
We assessed whether the intracellular bacterium Chlamydia pneumoniae w as present in post-mortem brain samples from patients with and without late-onset Alzheimer's disease (AD), since some indirect evidence see ms to suggest that infection with the organism might be associated wit h the disease. Nucleic acids prepared from those samples were screened by polymerase chain reaction (PCR) assay for DNA sequences from the b acterium, and such analyses showed that brain areas with typical AD-re lated neuropathology were positive for the organism in 17/19 AD patien ts. Similar analyses of identical brain areas of 18/19 control patient s were PCR-negative. Electron- and immunoelectron-microscopic studies of tissues from affected AD brain regions identified chlamydial elemen tary and reticulate bodies, but similar examinations of non-AD brains were negative for the bacterium. Culture studies of a subset of affect ed AD brain tissues for C. pneumoniae were strongly positive, while id entically performed analyses of non-AD brain tissues were negative. Re verse transcription (RT)-PCR assays using RNA from affected areas of A D brains confirmed that transcripts from two important C. pneumoniae g enes were present in those samples but not in controls. Immunohistoche mical examination of AD brains, but not those of controls, identified C. pneumoniae within pericytes, microglia, and astroglia. Further immu nolabelling studies confirmed the organisms' intracellular presence pr imarily in areas of neuropathology in the AD brain, Thus, C. pneumonia e is present, viable, and transcriptionally active in areas of neuropa thology in the AD brain, possibly suggesting that infection with the o rganism is a risk factor for late-onset AD.