Every 67 seconds another person develops Alzheimer’s in the U.S. More than 5 million Americans have Alzheimer’s disease. If that number was not scary enough, it is expected to rise to about 16 million in the next few decades. With such a dismal future, a new study that reversed Alzheimer’s symptoms in mice is a promising breakthrough.
A group of mice displaying Alzheimer’s symptoms had those symptoms reversed after being given a compound developed by researchers at St. Louis University in Missouri, according to a new study published in the Journal of Alzheimer’s Disease. The study looked at the use of antisense compounds for reducing brain inflammation and helping with memory revival. Antisense is molecule strand that, through a string of events, binds to RNA and eventually switches off some genes. The researchers’ specifically looked at whether a particular molecular compound, using antisense oligonucleotide (OL-1), could prevent amyloid beta plaques from forming in the brain, which would be of therapeutic value in treating Alzheimer’s.
Alzheimer’s is a degenerative mental disease that causes problems in humans with memory, thinking and behavior. The mice that the scientists used for their study were genetically engineered to overproduce human the amyloid beta protein to simulate having Alzheimer’s disease. They also used a wild strain of mice, which served as the control group. The wild strain mice were given random antisense. Half of the genetically engineered mice also received random antisense, whereas the other half received the OL-1. All the mice were given various tests to measure their memory, learning and behavior. The tests included things like going through a maze, exploring an unknown location and ability to recognize an object. The research team found that memory and learning did improve in the genetically engineered mice that received OL-1, particularly when compared to the genetically engineered mice that were given the random antisense. The memory and learning demonstrated by the genetically engineered mice that received OL-1 was similar to the memory and learning shown by the wild mice that received random antisense.
The results clearly showed that the molecular compound did restore learning, memory and appropriate behavior in a mouse model of Alzheimer’s disease. Conducted by a team led by Susan Farr, Ph.D., research professor of geriatrics, the study is the second using mice that demonstrates the value of an antisense compound in treating humans with Alzheimer’s disease.
As Alzheimer’s disease progresses in humans, nerve cells in brain areas that control language, sensory processing, reasoning, and conscious thought die because of the plaque deposition. They also find it difficult to learn new things, carry out multi-step tasks (even getting dressed) and cope with new situations, which the study simulated in the mouse tests.
In talking about the study’s findings, Farr noted that they reinforce the importance that the amyloid-beta protein plays in the Alzheimer’s disease process. The findings suggest that using an antisense compound that targets amyloid-beta protein and stops it from forming plaque in the brain should be further explored as a possible means for reversing Alzheimer’s disease symptoms. The scientists are hopeful that this could be a breakthrough in treating memory-related diseases and eventually lead to a means for retaining intelligence in individuals with cognitive decline.
By Dyanne Weiss