The brain may experience a notable change around age 50, when protective immune cells begin to decline and are increasingly replaced by cells carrying stronger inflammatory signals, according to new research. The findings may help explain why aging raises the chances of neuroinflammation and neurodegenerative disease, including dementia.

Researchers from the University of California, San Diego, the New York Genome Center, and the University of California, Irvine, conducted the study. Their work focused on changes involving immune cells in the brain during adulthood.

The team analyzed postmortem tissue from the hippocampus, the part of the brain responsible for learning and memory. The tissue came from 40 neurologically healthy adults ranging from 20 to 95 years of age.

Nathan Zemke, Ph.D., the first author and principal investigator at the UC San Diego Center for Epigenomics, described the central finding. The shift appeared to become especially notable after about age 50.

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"The most striking change was that after about age 50, the brain’s resident immune cells, called microglia, appear to be increasingly replaced by immune cells that enter from the bloodstream," Zemke told Fox News Digital.

Microglia normally help protect the brain by clearing debris and responding to injury, according to Zemke. "Microglia normally protect the brain by clearing debris and responding to injury, but the incoming cells carry stronger inflammatory signals."

The researchers believe this transition may contribute to chronic inflammation associated with cognitive decline and neurodegenerative diseases, including Alzheimer’s. However, the study did not establish that the cellular change causes cognitive decline or Alzheimer’s disease.

Researchers also observed deterioration among cells involved in maintaining the protective barrier between the blood and brain. That barrier serves as a filter that helps prevent harmful substances from entering the brain.

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The study further identified widespread changes in DNA and gene activity. Together, the findings offered researchers a closer look at biological changes that may occur in the aging hippocampus.

Zemke said one of the study’s most exciting implications involves the origin of the replacement immune cells. Because those cells come from the blood, they are more accessible than cells already located deep inside the brain.

He said it may eventually become possible to modify those cells so they are more protective and less inflammatory after entering the brain. Such an approach could offer a new way to address Alzheimer’s and other neurological diseases without directly manipulating cells within the central nervous system.

The findings remain in their early stages, Zemke emphasized. A better understanding of why the immune cell replacement occurs, and why it begins earlier in some people than in others, could lead to new strategies intended to preserve brain health during aging.

The study also had significant limitations because it examined postmortem brain tissue collected from different people across the adult lifespan. As a result, researchers could identify strong patterns connected with age, but they could not follow changes in the same person over several decades.

The research also could not prove that any particular cellular change causes cognitive decline or Alzheimer’s disease. In addition, researchers do not yet know what triggers immune cells from the blood to enter the brain.

Future research will need to examine whether changes involving the barrier between the blood and brain, inflammation, genetics, lifestyle, or other factors start the process. Zemke did not recommend any specific medical or lifestyle changes based only on the study.

"These findings are primarily about understanding the biology of brain aging and identifying new directions for prevention and treatment," he said. The timing and extent of the observed changes varied considerably among the people whose tissue was studied.

That variation suggests brain aging may not be a fixed process that unfolds in exactly the same way for everyone. "The next challenge is to understand what drives that variation and whether some of those factors can be modified," Zemke added.

The study was also limited by its small sample of 40 people and its focus exclusively on tissue from the hippocampus. Therefore, the results may not represent immune changes occurring throughout the entire brain.