A study on mice suggests a potential link between internal nasal tissue damage and heightened risk of dementia.
Researchers from Griffith University in Australia led a team investigating the role of Chlamydia pneumoniae, a bacteria known to infect humans and cause pneumonia. Notably, this same bacteria has also been found in a significant portion of human brains affected by late-stage dementia.
When internal tissues are damaged by nose picking, specific bacteria may gain easier access to the brain. This bacterial presence triggers a response within the brain that mimics some early signs of Alzheimer’s disease.
It’s important to note limitations in this research. Current findings are based on studies with mice, and further investigation in humans is necessary. However, these initial results hold promise for a deeper understanding of Alzheimer’s development, a currently unresolved medical puzzle.
The study investigated how the bacteria Chlamydia pneumoniae might travel to the brain. The research, conducted with mice, revealed the bacteria’s potential to ascend the olfactory nerve, which directly connects the nasal cavity and the brain. Additionally, damage to the nasal epithelium, the thin tissue lining the nasal cavity’s roof, was linked to worsened nerve infections.
This resulted in increased deposits of amyloid-beta protein within the mice brains. This protein is released in response to infections, and its plaque-like clumps are also prevalent in Alzheimer’s patients.
“We’re the first to show Chlamydia pneumoniae’s ability to travel directly from the nose to the brain, triggering pathologies resembling Alzheimer’s disease.”
“Our findings in mice are concerning and potentially relevant to humans as well.”
James St John from Griffith University (Australia)
The research team expressed surprise at the rapid migration of C. pneumoniae to the central nervous system in mice, with infection occurring within a 24-72 hour timeframe. This suggests the nose might be a potential pathway for bacteria and viruses to reach the brain quickly.
This research, while based on mice and lacking definitive human application, offers a valuable contribution to understanding Alzheimer’s disease, a common neurodegenerative condition. Further investigation into this promising lead is crucial.
Studies in humans are needed to confirm if the observed pathway functions identically. While the presence of these bacteria in humans is established, their route of entry remains unclear.
Nose picking is a common habit, with estimates suggesting up to 90% of people engage in it, along with many other species. While the benefits are uncertain, this study highlights the potential consequences and warrants a cautious approach.
The research team plans further studies to explore these processes in humans. In the meantime, St John and his colleagues advise against picking or plucking nose hairs due to the potential damage inflicted on protective nasal tissue.
A key question for future investigation involves whether the increased amyloid-beta deposits represent a natural and potentially reversible immune response upon infection clearance.
The complexity of Alzheimer’s disease is evident in the vast amount of ongoing research and the diverse approaches scientists employ to unravel the condition. Each study brings us closer to potential methods of prevention.
“While age remains a significant risk factor beyond 65, we are actively exploring environmental causes, including the potential role of bacteria and viruses.”
James St John
Abstract
Chlamydia pneumoniae is a respiratory tract pathogen but can also infect the central nervous system (CNS). Recently, the link between C. pneumoniae CNS infection and late-onset dementia has become increasingly evident. In mice, CNS infection has been shown to occur weeks to months after intranasal inoculation. By isolating live C. pneumoniae from tissues and using immunohistochemistry, we show that C. pneumoniae can infect the olfactory and trigeminal nerves, olfactory bulb and brain within 72 h in mice. C. pneumoniae infection also resulted in dysregulation of key pathways involved in Alzheimer’s disease pathogenesis at 7 and 28 days after inoculation. Interestingly, amyloid beta accumulations were also detected adjacent to the C. pneumoniae inclusions in the olfactory system. Furthermore, injury to the nasal epithelium resulted in increased peripheral nerve and olfactory bulb infection, but did not alter general CNS infection. In vitro, C. pneumoniae was able to infect peripheral nerve and CNS glia. In summary, the nerves extending between the nasal cavity and the brain constitute invasion paths by which C. pneumoniae can rapidly invade the CNS likely by surviving in glia and leading to Aβ deposition