Alzheimer’s disease currently affects more than 5 million Americans, with the numbers growing every year. This disease, which affects mostly Americans age 65 years old and above, is expected to triple in number by 2050. This may be a possibility unless more effective treatments and preventive medication are developed within that period. Researchers are now working to discover new ways to treat this disease, currently the 6th leading cause of death in the US. Recently, researchers have found a new compound that shows promise as a prevention drug against Alzheimer’s disease.
Researchers from the NYU Langone Medical Center have identified a compound called 2-PMAP that is showing promise as a future treatment drug for Alzheimer’s disease. The new compound has recently shown in animal studies to reduce the production of amyloid precursor proteins in the brain by more than half. Study findings are published in the journal Annals of Neurology.
Amyloid-beta proteins are known to be a common risk factor for Alzheimer’s. Studies indicate that the foundation of the disease is dependent on the clusters of amyloid-beta protein that accumulate in the brain. Because of this, amyloid-beta becomes a prime target for potential Alzheimer’s treatments.
Many clinical trials for treating Alzheimer’s disease fail because they try to tackle treatment for the disease after it has developed. During this time, severe damage to the brain has already started that symptoms begin to appear. Researchers believe that preventative measures may be a better option to keep the disease at bay. The objective is now preventing the disease from reaching a point where it begins to affect people.
Dr. Martin J. Sadowski, associate professor of neurology, psychiatry, and biochemistry and molecular pharmacology at NYU Langone, and colleagues looked into a library of compounds and found out that 2-PMAP reduced the production of amyloid precursor protein, considered as the mother protein for amyloid beta, by half. Dr. Sadowski, the lead researcher of the said study, and his team also found out that even low, non-toxic concentrations still reduced APP production by 50 percent or more in test cells.
The researchers then proceeded to see the effects of 2-PMAP on animal models. They found out that the compound have the same impact on APP and amyloid-beta in the brains in living mice. The mice models were genetically engineered to present the same genetic mutations found in Alzheimer’s patients, which causes an overproduction of APP and amyloid deposits in the brain. The researchers then provided the mice with a 5-day treatment of 2-PMAP. It was effective enough to lower the APP levels and, more importantly reduce amyloid-beta concentrations in the brain. DR. Sandowski and his team are now proceeding to making chemical modifications on 2-PMAP to improve its effectiveness.