Published on: Nov 21, 2025
Rutgers neuroscientist Peng Jiang’s renewed drive to combat Alzheimer’s disease traces back to an emotional conversation in his hometown of Qianshan, Anhui, China, where a neighbor described the painful moment when his mother — after nearly a decade of Alzheimer’s decline — looked at him without recognition and gently asked, How is your mother doing? The man broke into tears as he shared his fear that the disease, which runs in their family, might one day erase him from his own children’s memories.
This moment deeply affected Jiang, an associate professor in the Department of Cell Biology and Neuroscience at Rutgers School of Arts and Sciences and a member of the Rutgers Brain Health Institute, strengthening his urgency to find meaningful treatments in a field where no cure exists and therapeutic progress has been slow. Today, Jiang and neuroscience colleague Mengmeng Jin have announced a breakthrough that could transform how Alzheimer’s is understood and treated. Their new study, published in Nature Neuroscience, reveals that a rare mutation — CSF2RB A455D — appears to make brain immune cells naturally resistant to Alzheimer’s-related damage, pointing toward a new therapeutic direction centered on resilience rather than risk. Instead of trying solely to remove toxic proteins like amyloid or tau, the team explored how to reinforce the brain’s internal defense system, focusing on microglia, the immune cells responsible for clearing cellular waste, responding to injury, and protecting neurons. Using advanced stem-cell technology, the researchers generated human microglia with the protective mutation and transplanted them into mouse brains to create a chimeric model, then exposed the mice to Alzheimer’s-associated pathological proteins. The results were striking: microglia with the mutation retained youthful characteristics, avoided chronic and harmful inflammation, cleared toxic proteins far more effectively, and protected surrounding neurons from degeneration — all traits that microglia typically lose as Alzheimer’s progresses. Even more surprising, when mutated and unmutated microglia were placed together in Alzheimer’s environments, the mutated cells gradually dominated, while the unmutated ones weakened and stopped functioning properly; over time, the mutated microglia effectively refreshed the brain’s immune system, creating a healthier cellular landscape resistant to neurodegeneration. Importantly, this protective effect was observed not only in cells from individuals with Down syndrome (who have a significantly higher risk of early-onset Alzheimer’s) but also in cells from the general population, suggesting that the mutation may represent a universal mechanism for resilience.
The discovery opens doors to multiple potential treatment strategies, including transplantation of microglia engineered with the protective mutation into patients’ brains or the use of gene therapy to introduce the mutation into existing microglia to rejuvenate their function and enhance disease resistance. Researchers believe this immune strengthening approach could complement — or even surpass — traditional anti-amyloid therapies. The study involved major collaborative efforts, with contributions from Rutgers researchers Ziyuan Ma, Rui Dang, Haiwei Zhang, Rachael Kim, and Ava Papetti, and additional participation from scientists at the University of California, Irvine; Gladstone Institutes; Florida International University; and Nanjing Medical University. Jiang says the discovery is a step toward a future in which Alzheimer’s might be fought not just by targeting proteins that cause damage, but by enhancing the brain’s natural ability to protect itself.
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