Recently, scientists have begun delving into the link between Alzheimer’s disease and the immune system — an area of research that has grown trendier in recent months. One recent study suggested that certain central nervous system lymphatic system vessels did not properly remove buildup of plaque before reaching the brain.

Now, a new study published in Nature Neuroscience further examines the link between dementia and the immune system, concentrating on Alzheimer’s genetic risk factors and how they impact a specific type of immune cell. The researchers hope their work will pave the way for future research and potential treatments.

“There’s an emerging theme in Alzheimer’s genetics that the immune system may be strongly involved in the onset of Alzheimer’s disease,” Dr. Philip De Jager, director of the Program in Translation NeuroPsychiatric Genomics at the Ann Romney Center for Neurologic Diseases at Brigham and Women’s Hospital (BWH), said in the press release. “Before genetic studies, many thought that inflammation was a symptom of or a reaction to the disease, but our study and others build a compelling case that the immune system may be involved in the development of Alzheimer’s disease.”

In the study, the researchers analyzed blood samples from 100 young, healthy participants and did the same for 61 older people. They measured the protein levels in monocytes, immune cells that travel throughout the entire body — at times ending up in the brain as well. Once in the brain, monocytes can transform into macrophages, which are designed to adjust to their new environment (such as the nervous system).

The researchers focused specifically on a certain protein known as TREM2, one that has previously been associated with Alzheimer’s. Past research has in fact found that mutations in the TREM2 gene could contribute to Alzheimer’s disease, and some current drugs target it. De Jager and his team reinforced that higher levels of TREM2 indeed lead to an increased risk of Alzheimer’s, and that a genetic variant of a separate protein called CD33 could affect TREM2 levels.

“Up until now, it’s been unclear whether it would be beneficial to increase or decrease TREM2 levels,” Elizabeth Bradshaw, a co-author of the study, said in the press release. “Further studies are needed to understand the connections we’re uncovering and the roles of these proteins, but we’re clearly seeing evidence that these genetic variants have an effect in this type of immune cell.”

Researchers aren’t entirely sure what causes Alzheimer’s disease, but it’s typically believed to be a combination of genetic, lifestyle, and environmental factors. The disease is caused by the buildup of beta-amyloid in the brain, which damages and destroys brain cells, ultimately causing memory loss as well as other dementia-related issues. Making the connection between Alzheimer’s and the immune system is certainly ground-breaking, but more in-depth research will be needed to fully understand the link, and to learn how to properly target it in treatment.

Source: Chan G, White C, Winn P, Cimpean M, Replogle J, Glick L. CD33 modulates TREM2: convergence of Alzheimer loci. Nature Neuroscience. 2015.