When Professor Michal Schwartz began asking whether the brain and immune system talk to each other, most scientists thought she was wrong. The brain, after all, was supposed to be sealed off from the body's immune defenses. But Schwartz, a researcher at the Weizmann Institute of Science in Rehovot, Israel, believed something different—and she was right.
This month, her decades of work took a major step toward helping patients. A Phase I clinical trial of her experimental Alzheimer's therapy showed it is safe for human use, opening the door for larger studies that could eventually bring a new treatment to millions.
The approach is unusual. Rather than targeting the sticky amyloid plaques that build up in Alzheimer's brains, Schwartz's team focused on the immune system itself. Her earlier research revealed something surprising: the brain actually depends on immune cells for its lifelong health. When the immune system weakens with age—a process called immune aging—it can trigger harmful brain inflammation that speeds up dementia.
"Removing amyloid plaques is not sufficient to halt the disease," Schwartz explained. Her work suggested that fixing the broken immune system might be just as important.
Building on this discovery, Schwartz co-founded a company called ImmunoBrain. The company developed a drug called IBC-Ab002, an antibody designed to reverse immune aging in the brain. Although it works on the same molecular target as some cancer immunotherapy drugs, IBC-Ab002 was specifically engineered for Alzheimer's disease.
The Phase I trial enrolled 40 patients with early-stage Alzheimer's at 11 medical centers across three countries: five in the United Kingdom, five in Israel, and one in the Netherlands. The trial's main goal was to check whether the treatment was safe—and it was. Patients tolerated all tested doses without serious side effects. The drug also showed the biological activity scientists expected, meaning it behaved the way it was designed to.
Dr. Tommaso Croese, who led the clinical trial and was once a student in Schwartz's lab, said the results mark a turning point. "This finding suggested that removing amyloid plaques, long considered a hallmark of Alzheimer's, is not sufficient to halt the disease," he noted, reflecting on how Schwartz's work changed the field.
The results were published in Nature Medicine. Professor Catherine J. Mummery of University College London's Dementia Research Center also helped lead the study.
For Schwartz, who received the Israel Prize in Life Sciences for her research, this trial is proof that her ideas—once considered radical—are now moving toward the clinic. More research is still needed to see whether the treatment actually slows or improves memory loss in patients. But for the 55 million people living with dementia worldwide, this small trial represents genuine hope that science is finding new doors to open.