This research was supported by BrightFocus
Most people have had the experience of listening to a radio station with a weak signal. One solution is usually to turn up the volume. By increasing the signal, we hope that our brains will be able to discern more of the programming and filter out more of the noise.
This is analogous to how currently-approved Alzheimer’s disease drugs are designed. By adjusting the levels of chemical messengers used by neurons to communicate with one another, the drugs are intended to overcome some of the symptoms caused by Alzheimer’s disease. Unfortunately, they do so without ever addressing the underlying causes of the disease.
Recently, the BrightFocus Foundation awarded an Alzheimer’s Disease Research Fellowship to Soong Ho Kim, PhD, at Mount Sinai Hospital in New York City, to study whether a new drug could directly attack symptoms of the disease, but also work to address the disease process.
A new study in Molecular Psychiatry now provides evidence that this line of research may be progressing. Lead author Kim, working with colleagues at Mount Sinai and the University of California, showed that the experimental drug did exactly that when given to mice: improved symptoms and affected the disease process.
Using mice engineered to show symptoms similar to Alzheimer’s disease, researchers demonstrated that mice receiving the drug performed better than untreated animals in tests that measured learning and anxiety. When examined for soluble beta amyloid, the same animals showed reductions in levels of the protein.
Beta amyloid is a hallmark of Alzheimer’s disease, and is believed to be directly tied to damage of neurons. Seeing its reduction suggested that the new drug may be acting directly to reduce or repair damage caused by Alzheimer’s disease.
How the drug is working is not completely understood, but data presented in the same studies suggested that one of the drug’s benefits may be to help maintain the brain’s ability to replace lost neurons. This positions the new drug as a possible candidate for both therapeutic and preventative applications towards Alzheimer’s disease.
Alzheimer’s disease patients are often prescribed several drugs and may have other conditions for which they are being treated. Each of these drugs possess their own side effects and may interact with other drugs. This new class of drugs offers the exciting possibility of minimizing these concerns, while addressing a host of biological goals, all with a single drug.
“Alzheimer's patients suffer from memory problems and anxiety/depression,” noted Dr. Kim. “The drug has a potential to not only alleviate those symptoms but repair damaged brain by stimulating the generation of new brain cells and reducing the levels of the toxic substance called beta amyloid.”
BrightFocus spokesperson and Vice President of Scientific Affairs, Dr. Guy Eakin, said, “This project may well have been considered a long shot in a funding environment where even very conservative goals are left unfunded. We are very proud to have identified this team and project as capable leaders with their sights on lofty goals. The team is in a strong position to gather the resources they need to see this move to human clinical trials.”
Neurons are the core components of the brain and spinal cord of the central nervous system (CNS) that process and transmit information.
Amyloid is a general term for protein fragments that the body produces normally. Beta amyloid is a protein fragment snipped from an amyloid precursor protein (APP). In a healthy brain, these protein fragments are broken down and eliminated. In Alzheimer's disease, the fragments accumulate to form hard, insoluble plaques.