pneumoniae bacteria have also been isolated from some post-mortem patient brains 7. It is now well known that Aβ is an antimicrobial peptide, released by neural cells in response to infectious agents 12, 13, so it is not surprising that the presence of bacteria in the brain can result in Aβ deposition reviewed in 8. pneumoniae antigens were found in proximity to classical hallmarks of late-onset dementia pathology senile plaques, amyloid beta (Aβ) deposits and cells containing neurofibrillary tangles in the cerebral cortex and hippocampus. pneumoniae in brains from patients with late-onset dementia has also been shown using immunohistochemistry, where C. pneumoniae DNA was found in 80% of patient brains, compared to 11% of control brains 11. pneumoniae DNA, compared with only 5% of control age-matched brains 9, 10. In the late 1990s, it was shown that 90% of such post-mortem patient brains contained C. pneumoniae in post-mortem brains from late-onset dementia patients. ![]() Several key studies have reported the presence of C. pneumoniae primarily infects the pulmonary and nasal mucosa, but has in recent years been linked to diseases distinct from the respiratory tract, such as atherosclerosis/coronary disease 3, asthma 4, inflammatory arthritis 5, multiple sclerosis 6 and, in particular, late-onset dementia (late-onset Alzheimer’s disease) 7, 8. pneumoniae can rapidly invade the CNS likely by surviving in glia and leading to Aβ deposition.Ĭhlamydia pneumoniae is a gram-negative respiratory pathogen, responsible for causing 5–20% of community-acquired pneumonia 1, 2. In summary, the nerves extending between the nasal cavity and the brain constitute invasion paths by which C. pneumoniae was able to infect peripheral nerve and CNS glia. Furthermore, injury to the nasal epithelium resulted in increased peripheral nerve and olfactory bulb infection, but did not alter general CNS infection. pneumoniae inclusions in the olfactory system. Interestingly, amyloid beta accumulations were also detected adjacent to the C. pneumoniae infection also resulted in dysregulation of key pathways involved in Alzheimer’s disease pathogenesis at 7 and 28 days after inoculation. pneumoniae can infect the olfactory and trigeminal nerves, olfactory bulb and brain within 72 h in mice. pneumoniae from tissues and using immunohistochemistry, we show that C. In mice, CNS infection has been shown to occur weeks to months after intranasal inoculation. ![]() pneumoniae CNS infection and late-onset dementia has become increasingly evident. Chlamydia pneumoniae is a respiratory tract pathogen but can also infect the central nervous system (CNS).
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