he team suspects the involvement of brain cells called microglia, the major immune cell that rushes to injury sites and helps repair and clean up wounds in the brain.
The work is the latest in a growing body of research that is trying to determine the exact role of inflammation in Alzheimers disease. OBanion notes that some studies have found that taking medications to squelch inflammation, such non-steroidal anti-inflammatory drugs or NSAIDs, might help reduce a persons chances of getting Alzheimers disease, while other studies, including a study of more than 2,100 people published in April, refute that notion.
There is a great deal of evidence that inflammation plays a potentially negative role in Alzheimers disease, said OBanion. But much of the evidence comes from experiments with cells in a dish or postmortem human tissue, not from living organisms in which disease progression is closely monitored.
People have talked for a long time about a balance of good guys and bad guys within the inflammatory process, either causing harm or alleviating the disease. The current work reinforces the idea that inflammation is not simply the bad guy that many people think it is.
The work could have ramifications for the development of a vaccine or other strategy to protect against or fight off Alzheimers. Work on an Alzheimers vaccine has at times been promising, reducing the number of plaques in the brains of animals and a few people with the disease, but its also been fraught with difficulty, producing side effects such as encephalitis or severe brain inflammation in people with Alzheimers.
The potential to treat Alzheimers disease by modulating the immune system is tremendous and is an area that has not been fully explored, said OBanion. That said, people have to remember that the current findings are in mice, not people. We need to be cautious about how to interpret the results.
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