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New Research Reveals Alzheimer’s May Start From Bacteria From the Nose

Research from both Griffith University and the Queensland University of Technology found some alarming evidence as part of their research into how the bacteria Chlamydia pneumoniae can reach the brain, as it appears that these microorganisms can enter the brain through nerves in the nasal cavity, which they say may set off a series of events that may lead to diseases like Alzheimer’s.

“Our work has previously shown that […] several different species of bacteria can rapidly, within 24 hours, enter the central nervous system via peripheral nerves extending between the nasal cavity and the brain,” said associate professor and primary author Jenny Ekberg, whose work alongside colleagues was published in the journal Scientific Reports. “With this background knowledge, we were able to track how this new bacterium [C. pneumoniae] can also sneak past the blood-brain barrier and quickly enter the brain.”

The series of nerves that help in our olfactory function are in close proximity to the brain, leading a team of researchers to believe that this may be a possible pathway for bacteria to enter the brain and trigger a series of events that may lead to Alzheimer’s disease. (Lynch, 2006)

C. pneumoniae was said to often cause respiratory tract infections; however, a statement from the Griffith University press release describes the bacteria as also having been found in the brain, which raises questions on whether or not it can wreak havoc on our central nervous system.

Tests performed on mouse models revealed that within 72 hours after introducing the bacteria to mouse noses, C. pneumoniae may infect nerves within the nose, such as the olfactory and the trigeminal nerves. Then, the bacteria climb their way to the olfactory bulb—and it’s a short distance towards the brain from there.

Once these bacteria enter the central nervous system, the brain reacts by depositing beta amyloid plaques which nestle between nerve endings, the onset of which being a common feature among patients with Alzheimer’s disease. Additionally, these bacteria infect glial cells near the olfactory nerve, which the authors say may be how the bacteria persists within the nervous system after initial infection.

The image above shows histopathology, or tissue diagnosis, of Alzheimer’s disease in an area of the hippocampus, with beta-amyloid plaque buildup shown with the arrows. (Häggström, 2020)

 “These cells are usually important defenders against bacteria, but in this case, they become infected and can help the bacteria to spread,’’ said Ekberg. “We have suspected for a long time that bacteria, and even viruses, can lead to neuroinflammation and contribute to [the] initiation of Alzheimer’s disease, however, the bacteria alone may not be enough to cause disease in someone. Perhaps it requires the combination of […] genetic susceptibility plus the bacteria to lead to Alzheimer’s disease in the long term.”

Ekberg and the research team mention that their potentially alarming discovery has given them “the drive to urgently find treatments to stop this contributing factor to Alzheimer’s,” especially given their belief that the results in mice models are translatable to humans given the similarities in our nervous systems.

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