Researchers in New York have found a way to slow down Alzheimer's-related memory loss and improve learning, following a successful experiment on mice.
The idea is to remove harmful beta-amyloid plaques, which are protein deposits in the brain that are a hallmark of Alzheimer's disease.
The researchers relied on an insulin-regulating protein called PTP1B, discovered by Professor Nicholas Tonks in 1988, which is currently used as a target for treating obesity and type 2 diabetes, both of which are risk factors for Alzheimer's disease.
The experiment showed that giving mice drugs that inhibit this protein led to the removal of harmful plaques from their brains, which in turn improved learning and memory. "The goal is to slow the progression of Alzheimer's disease and improve the quality of life for patients," Tonks said in a statement. (PTP1B "stops" or reduces the activity of immune cells in the brain when it increases, allowing plaques to accumulate. By inhibiting it, these cells' ability to clear the brain is improved, which may help in combating Alzheimer's.)
The study included mice aged between 12 and 13 months, which were given the DPM-1003 inhibitor at a dose of 5 milligrams per kilogram twice a week, and the experiment lasted for five weeks.
The mice underwent a series of behavioral tests, including object recognition and a water maze, and then their brains were dissected to assess plaque levels.
The results revealed that the PTP1B protein interacts directly with another protein called spleen tyrosine kinase, which regulates immune cells in the brain to remove harmful waste, including excess plaques.
Graduate student Yuxin Sen explained: "As the disease progresses, these cells are depleted and become less effective. But inhibiting PTP1B improves the performance of immune cells, which helps remove plaques."
Tunks and his team are working with the pharmaceutical company DepYmed to develop protein inhibitors, which they believe could be combined with existing Alzheimer's treatments. The researchers explained that the need for additional therapies is urgent, as the number of cases is expected to nearly double by 2050.
