A new study published in the Science Translational Medicine Journal on May 25, suggests that Alzheimer’s disease may be the product of the body’s attempt to fight microbial infections. Scientists from Harvard discovered that a protein called is thought to cause neuronal death in Alzheimer’s disease.

This study is the first to contradict the traditional theory of Alzheimer’s disease that states that a protein (amyloid beta) builds up plaque in the brain that destroys some nerves and connections, what ends in memory loss. This study claims that the protein may be just the response of the human immunosystem to protect the brain from infections.

Alzheimer's disease new theory
Scientists from Harvard suggest that Alzheimer’s disease may be the product of the body’s attempt to fight microbial infections. Credit: Newsclip.com

The study analyzed the vulnerability of people to infections, and the ability of those diseases to reach the brain, triggering problems at a neurological level that lead to the disease.

Amyloid beta: Friend or enemy?

The protein related to Alzheimer’s disease has been perceived as a useless waste product in the brain cortex. However, this study considers that instead, is the natural response from the neurological network to protect the brain from infections.

Tha protein known for damaging brain cells and deteriorate cognitive responses may be the mechanism of protection from invading microbes, what is a major and crucial task. In that sense, is a part of the brain’s immune system. The level of sophistication in the protein may be the main reason why scientists have not detected its function before.

Microbial cells can be dangerous to the brain’s normal functioning, and the immune system, recognizing that, creates a formula to protect itself from the harmful effects infections can cause. The problem is when the protein has harmful effects on its own. The study could not determine whether the protein can be manipulated to avoid its hazard potential.

Scientists discovered it through a multiple-phase study

The mechanism to execute the investigation was to infect human and hamster cells with fungi and microbes to study the response of the immune system. Through observation, they realized that amyloid beta was produced and it had a protective effect on the cells since almost half of them were not infected with the microbes.

The second version of the study involved data from nematodes who received doses of amyloid beta and were infected with fungus. The roundworms survived more than expected. The final step of the study was with mice, who were genetically modified to overproduce a human form of amyloid beta and then infected with the meningitis bacteria. Mice with amyloid beta faced the disease twice as long as those that did not have the protein.

Through the investigation, scientists also observed that the protein amyloid beta formed itself around the bacteria, creating a sort of trap with rapidly established plaques.

The new theory could change the way science understands Alzheimer’s

If these results are proved correct in time, with more investigation, the entire medical understanding of Alzheimer’s disease will change. In that sense, to recognize the protein as a natural mechanism of protection, scientists could detect risk in medical profiles, considering the vulnerability of a patient to infections that may lead their immune system to overproduce amyloid beta.

The explanation made by Harvard’s investigators is that older people have weaker immune systems, with compromised mechanisms of protection of the brain. In that sense, the trend to get infected with microbes is constant, what can make the brain create more and more protein to protect from those pathogens.

The Scientific American Journal published some considerations made by scientists that were not a part of the study.

“These results are particularly intriguing, previous [research] shows that several infectious agents, including viruses, trigger amyloid beta production and accumulation. It is possible to speculate that during a mild infection the production of amyloid beta may help, but in the presence of persistent or repeated infections, amyloid beta levels may accumulate, exceeding a threshold. In this case its protective role might change to the well-known neurotoxic one,” said Anna Palamara, a microbiologist at the Sapienza University of Rome.

Until more investigations are made on the topic, the approach to the protein in the pharmaceutical sense is still blurry. Potential treatments can be built up upon these new considerations, by not trying to discard the formation of the protein but to reduce it enough to allow still its protective role to develop. Another possible path to restructuring the treatment is to attack the mechanisms of microbes to reach the brain cells, to create a synthetic mechanism of diminishing the threat. That would avoid the immune system’s natural response to form plaques of amyloid beta.

The next step if to make the scientific community embrace these findings and to keep up with the research as long as possible. The goal is being able to determine the microbes that represent the most severe threat to the immune system, as well as the behavior in the aging brains.

Source: Science Mag