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By Maria Azzurra Volpe
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Scientists have just found a way to restore part of the brain’s immune response and reduce abnormal nerve-cell activity linked to Alzheimer's disease.
The study, led by Professor Minah Suh of the department of biomedical engineering at Sungkyunkwan University, in collaboration with the biotechnology company IMNEWRUN and Professor Ho-Keun Kwon's team at Yonsei University College of Medicine, focused on the brain’s own immune cells.
These cells, known as microglia, normally act as the brain’s first responders, helping to detect and respond to damage while maintaining a healthy surrounding environment.
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But in Alzheimer's disease, that response becomes impaired. At the same time, nerve cells can become unusually active.
According to the study, published in Science Advances, that disruption is linked to changes in two immune-regulating proteins, PD-1 and PD-L1.
In mice used to model Alzheimer’s disease, the researchers found increased levels of PD-1 in microglia and increased levels of PD-L1 in astrocytes, cells that help maintain the brain environment.
To investigate what these changes were doing, the researchers directly administered an antibody that blocks PD-L1 into the brains of the Alzheimer’s model mice. They then used advanced microscopy techniques to observe living brain cells.
The results were striking: the microglia regained their ability to respond properly to damaged areas, while the excessive activity of neurons was reduced.
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Commenting on the findings, Dr. John Showalter, chief operating officer of Linus Health, who was not involved in the study, told Newsweek that the research adds to growing evidence that the immune system plays a significant role in Alzheimer's disease and dementia.
"One of the clearest pieces of evidence that the immune system is involved is that individuals who receive the shingles vaccine are less likely to develop dementia.
"This study indicates that immune cells (specifically microglia) may be directly involved in the process and is likely to increase interest in immune-mediated research," he said.
The effects were stronger when PD-L1 was altered directly in the brain than when the antibody was given through the body.
The findings suggest that disrupted immune signaling could be linked to changes in how the brain responds to damage and excessive activity in neurons. The researchers propose that abnormal immune regulation may prevent microglia from behaving normally, contributing to an unhealthy brain environment.
The study also reflects a broader trend in Alzheimer's research: "Anti-amyloid and anti-tau drugs make up only 25 percent of the drugs/therapies that are currently in randomized clinical trials," Showalter said.
"Inflammation and immune-modifying medications make up 18 percent vs anti-amyloid at 16 percent. The breadth of possible ways to treat Alzheimer's disease and cognitive impairment is extremely exciting."
However, the findings do not show that blocking PD-L1 treats or cures Alzheimer’s disease in humans. The research was conducted in mice with an Alzheimer’s-like condition, so the results represent evidence for a possible approach rather than an established treatment.
Showalter said one of the biggest obstacles to turning these findings into a treatment is how the antibodies would be delivered to patients.
"The biggest challenges found in this study are about the ability to administer the antibodies like a medication," he said, adding that it would be "very risky to inject a medication/antibody directly into the fluid that surrounds the brain and spinal cord."
Further research would be needed to determine whether the same effects could occur in humans.
Reference
Taeyoung Park et al, Targeting glial PD-1/PD-L1 restores microglial homeostasis and reduces neuronal hyperactivity in an Alzheimer's disease model, Science Advances (2026). DOI: 10.1126/sciadv.adx0731
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