Dramatic improvment when given immune cells
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Researchers at the University of California Riverside (UCR) and the University of South Florida have found evidence that weakened or suppressed immune responses may be responsible for Alzheimer’s disease and that boosting the immune system of Alzheimer’s mice with cells from normal mice causes dramatic improvement in learning and memory. The findings, by Professor Douglas Ethell, assistant professor in the Biomedical Sciences Division of UCR in collaboration with Professor Gary Arendash of the Johnnie B. Byrd Institute and University of South Florida, were released this week by the prestigious journal Neurobiology of Disease. This new research is based on a 2002 report by Professor Ethell that found that beta-amyloid, a protein, increases the amount of the immune suppressor, Fas ligand, and that prolonged suppression of immune responses to that protein is implicated in Alzheimer’s disease. Ethell wondered if boosting immune responses to beta-amyloid could improve learning and memory in mice that develop Alzheimer’s. He teamed up with Arendash who had previously shown that vaccinating mice with beta-amyloid caused temporary improvements in Alzheimer’s mice. However, clinical trials with beta-amyloid vaccinations had been halted due to brain inflammation in some patients. In this study, however, Ethell and Arendash tried a different approach. They injected the Alzheimer’s mice with just the immune cells from normal mice that had been vaccinated with beta-amyloid. The researchers found that with just one injection the mice did significantly better on memory tests and that the improvements lasted one to two months after receiving the cells, which was the longest time-point they tested. Findings from this study may shift the search for an Alzheimer’s cure away from beta-amyloid injections. Instead, the research suggests that a subtle shift in immune responses to the protein may be all that is required for the development of an effective therapy for Alzheimer’s. “We believe these findings show that resetting the responsiveness of specific immune cells to beta-amyloid can provide an effective therapeutic approach to treating Alzheimer’s disease,” Ethell said. “Translating this research into the clinic may involve isolating immune cells from a compatible donor, expanding them in the lab and delivering them to an Alzheimer’s patient. As we learn more about these cells, it may be possible to isolate them from the Alzheimer patient’s own blood, reactivate them in the lab and then return those cells to the patient.”

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