Inflammation May Contribute to Development of Alzheimer’s Disease

Our immune system keeps guard over our body, fending off pathogens and doing its best to prevent viruses and bacteria from causing diseases. Since all systems in the body are interconnected and cooperate, it is no wonder that the nervous system can be affected by processes in organs other than the brain. According to scientists, inflammation can contribute to development of Alzheimer’s disease.

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A bit of science

When our body encounters a virus or some other pathogen for the first time, it does not know it and has no antibodies to curb its activity. If a disease is contracted, the immune system initiates a cascade of complex processes that have the same goal of eliminating the intruder from the body’s ecosystem. The next time the pathogen gets into your bloodstream, it will be attacked by immune system cells fast. This mechanism is called adaptive immunological memory and is carried out by such cells belonging to the immune system as B and T lymphocytes.

However, it is not the only line of defense. There is the innate immune system comprised of macrophages, monocytes, and NK cells, which does not share the same properties that would enable it to ensure antigen specificity, but turns out to be able to remember the pathogens the body has already encountered. Termed “trained immunity”, the system has been highlighted only recently and has the potential to shift the paradigm. Until recently, it was believed that only the adaptive memory can remember previous cases of disease, but it appears that the innate immune system has such a capacity too, as fighting pathogens triggers epigenetic changes, which are not that long-lasting but still capable of playing a significant role in building resistance to infection.

Although all this information may seem not to be relevant to neurodegenerative diseases, including Alzheimer’s disease, it appears that acute immune training causes changes in the brain that can stimulate processes of amyloid beta plaque formation – a factor considered to be a major contributor to Alzheimer’s disease development.

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Long-lasting effects

A team of researchers from several German educational institutions and research centers, including the University of Tübingen, the University of Bonn, etc., carried out a study aimed at finding out whether innate immune memory can affect neuropathology. They focused on the long-lived immune cells found only in the brain, which are called microglia.

To find out what microglia response follows an encounter with a pathogen, the scientists injected Alzheimer’s disease mouse models with lipopolysaccharide, which is a bacterial component that, once it has got into the body, induces inflammation. The microglia learned what the pathogen is like and were ready for another invasion. After subsequent infections, there was no response, as the cells developed tolerance to the pathogen.

The researchers found that the first injection, which induced inflammation and after which the innate immune system cells were deployed, accumulation of amyloid plaques was accelerated. However, the effect was observed only in the group of mice that received only one injection. In those rodents that received four injections, the levels of beta-amyloid were even lower than in those that did not receive any injections at all.

The study findings suggest that inflammation could be a contributor to development of Alzheimer’s disease, as it promotes formation of amyloid plaques. However, more research is needed, as the processes are complex and remain a riddle.

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