Researchers at Cold Spring Harbor Laboratory on Long Island have discovered a potential approach to slowing memory loss in Alzheimer’s disease by suppressing the protein PTP1B. The study, published in the Proceedings of the National Academy of Sciences, found that mice with Alzheimer’s disease symptoms showed “improved cognitive behaviors” when PTP1B was suppressed.
The research focused on amyloid-beta, or plaque, which accumulates in the brain and is a key factor in Alzheimer’s development. By reducing PTP1B, researchers found that the amyloid-beta burden decreased and cognitive function improved. Mice treated with a PTP1B inhibitor showed a 30% to 50% reduction in amyloid burden. Using standard behavioral tests, the research demonstrated clear impacts on learning and memory. In tests where mice learned to locate a platform in a pool, treated Alzheimer’s mice performed similarly to normal mice, while untreated Alzheimer’s mice were unable to learn or remember the platform’s location. In another test, treated mice showed curiosity about new objects similar to normal mice, whereas untreated Alzheimer’s mice did not recognize objects as new.
Nicholas Tonks, lead author and professor at Cold Spring Harbor Laboratory, noted that the goal is to “slow Alzheimer’s progression and improve quality of life of the patients.” According to the Alzheimer’s Association, more than 7 million people age 65 and older in the United States are estimated to have the disease. Despite the promising results, Tonks emphasized that it takes years, clinical trials, and much more funding before such treatments can reach patients.
Currently, there are a few medications that reduce amyloid accumulation in people with early Alzheimer’s disease, slowing progression by roughly 30% over 18 months. A successful treatment based on this research could provide another option, allowing patients to maintain their functioning for much longer. Dr. Nikhil Palekar, director of the Stony Brook Center of Excellence for Alzheimer’s Disease, called the lab’s research “novel” and noted that other Alzheimer’s mechanisms—such as tau protein and brain inflammation—also require attention, but expressed hope that findings like this could translate to human treatments.
This article is an AI-assisted summary. All facts and figures are drawn from the original report: https://www.newsday.com/news/health/alzheimers-disease-brain-protein-mice-improved-memory-o32ntsm3