New Alzheimer's Breakthrough: Drug Slows Memory Loss in Mice by Clearing Brain Plaques
Researchers in New York have made a significant advance in the long fight against Alzheimer's disease, uncovering a method to slow memory loss and enhance learning capabilities in mice. This development centres on the clearance of harmful amyloid beta plaques, the protein fragments that accumulate in the brain and are a defining characteristic of this irreversible and incurable form of dementia, which affects over 7 million Americans.
The key mechanism involves an insulin-regulating protein known as PTP1B, originally discovered by corresponding researcher and professor Nicholas Tonks in 1988. This protein is already a recognised target for treating obesity and type 2 diabetes, both of which are risk factors for Alzheimer's. By administering inhibiting drugs to mice, the researchers successfully removed these damaging plaques from their brains.
Mouse Maze Experiments Reveal Promising Results
In the study, all test subjects were mice aged 12 to 13 months. They received the inhibitor DPM-1003 at a dosage of five milligrams per kilogram of body weight twice weekly over a five-week trial period. During this time, the mice underwent a series of cognitive assessments, including object recognition tests and water mazes, to evaluate their memory and learning abilities. Following the trial, the mice's brains were dissected to measure plaque levels.
The findings provided crucial insights into how the PTP1B protein interacts directly with another protein called spleen tyrosine kinase in the brain. Normally, spleen tyrosine kinase helps regulate the brain's immune cells to clear out debris such as excess plaques. However, as graduate student Yuxin Cen explained, "Over the course of the disease, these cells become exhausted and less effective." The research indicates that inhibiting PTP1B can rejuvenate these immune cells, enhancing their function and facilitating the clearance of amyloid beta plaques.
A Hopeful Future for Alzheimer's Treatment
Professor Tonks and his team are now collaborating with the pharmaceutical company DepYmed, Inc. to develop these inhibitors further. Tonks emphasised that existing Alzheimer's therapies could potentially be combined with these new drugs, addressing a critical need for additional treatments. With Alzheimer's cases projected to nearly double by 2050, the urgency for effective solutions is immense.
Reflecting on the personal impact of the disease, Tonks, whose mother lived with Alzheimer's, described it as "a slow bereavement. You lose the person piece by piece." The ultimate goal of this research, he stated, is to slow the progression of Alzheimer's and improve the quality of life for patients, offering a beacon of hope in the ongoing battle against this devastating condition.
