Chlamydophila pneumoniae, a bacterium that normally infects the respiratory tract, can also enter the brain and cause Alzheimer's disease, Australian scientists have found. The bacteria travel to the brain along the nerves and lead to the formation of beta-amyloid deposits and the activation of genes associated with Alzheimer's disease. Now researchers are looking for a way to reduce the likelihood of chlamydia entering the brain, and are also working on a drug that will get rid of those that do get there. The main causative agent of pneumonia in humans is the bacterium Chlamydophila pneumoniae. They can also cause damage to the upper respiratory tract (laryngitis, sinusitis, bronchitis, etc.) and may be associated with the development of asthma, atherosclerosis, and even autoimmune diseases. The bacteria can only spread from person, so outbreaks of chlamydial respiratory tract infections usually occur in close communities. In 70% of those infected with C.pneumoniae, it can remain asymptomatically in the mucous membranes of the upper respiratory tract for months, including after the infection.
C. pneumoniae has previously been found in the brains of people who died at an advanced stage of dementia. The bacteria were observed in 90% of such people and only 5% of those who died at the same age without signs of dementia. However, there were also enough studies in which no connection between C. pneumoniae and dementia was observed, so it was still unknown whether these bacteria are able to influence the functioning of the nervous system. Researchers from the Australian Griffith University selected 12 mice for the experiment, which were injected with a solution with C. pneumoniae nasally, and five mice as a control group, which received saline. Mice were euthanized on the 1st, 3rd, 7th and 28th day of the experiment, step monitoring the changes that took place in their body. The scientists described their findings in an article in the journal Scientific Reports.
The bacteria were indeed able to enter the cells of the olfactory nerve and then reach the brain.
Damage to the epithelium in the nose increased the concentration of bacteria in the olfactory bulb and trigeminal nerve, but did not significantly affect their number in the brain.
“We have previously found that several different types of bacteria can quickly, within 24 hours, enter the central nervous system through the peripheral nerves that run from the nasal cavity to the brain,” the researchers say. “Based on this knowledge, we tracked how C. pneumoniae also crosses the blood-brain barrier and gets to the brain.”
When the bacteria entered the brain, over the next few days, its cells reacted by forming beta-amyloid deposits, which are considered a hallmark of Alzheimer's disease. After a couple of weeks, the genes involved in the development of Alzheimer's disease were sharply activated.
“We have long suspected that bacteria and even viruses can lead to inflammatory processes in the nervous system and contribute to the onset of Alzheimer's disease,” the authors of the work say. “However, bacteria alone may not be enough to cause disease in humans.
It may take a combination of genetic predisposition and bacteria to lead to Alzheimer's disease in the long term. Now that we have new evidence, it gives us an incentive to urgently find treatments to combat this Alzheimer's contributing factor.”
In addition, the bacteria infected glial cells, the supporting cells of the nervous tissue. Obviously, this is what allowed the bacteria to persist in the nervous system for a long time.
“Normally, these cells protect the brain from bacteria, but in this case they become infected and possibly help the bacteria spread,” the scientists note.
“Based on our results, we conclude that the nerves that run between the nasal cavity and the brain represent pathways by which C. pneumoniae can quickly enter the CNS and cause long-term genetic and molecular changes that may contribute to the onset of Alzheimer's disease.” — conclude the authors of the work.
Although the study was done in mice, the same nerves are present in humans, and it is likely that the infection spreads will be similar, the scientists explain. Now they are looking for drugs that will help glial cells get rid of bacteria in the brain, as well as developing a drug that will prevent C. pneumoniae from entering nerve cells.
The mice were observed for only a month, so it is not yet clear what kind of long-term consequences infection can lead to. It remains to be seen how long the bacteria can live in the brain, what damage they can do in that time, and how this damage can affect the state of the brain.
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