A Group of Researchers were Successful in Reversing the Alzheimer’s disease Symptoms Using A New Compound

Around 5 million individuals in the US have Alzheimer’s disease, and this is approximated to increase to 16 million by 2050. Such numbers point out the significance of discovering new therapies for the Alzheimer’s disease, and new study from Saint Louis University could provide just that. In a mouse research, scientists were capable to reverse Alzheimer’s disease symptoms using a novel molecular compound.

The team lead by Susan Farr developed a substance known as antisense oligonucleotide (OL-1). When examined on mouse models with Alzheimer’s, they identified the compound reversed classic symptoms of the Alzheimer’s disease – brain soreness and learning and memory failures.

The scientists describe that OL-1 works by preventing messenger RNA (mRNA) that promotes the production of excess amyloid-beta protein, which can led to the growth of amyloid-beta plaques – a hallmark of Alzheimer’s disease.

In detail, OL-1 was capable to decrease the overexpression of the amyloid-beta protein precursor gene, which manages the quantity of amyloid-beta protein existing in the body.

Compound examined on human amyloid-beta gene

To reach their findings, lately published in the Journal of Alzheimer’s Disease, the group tested OL-1 on genetically engineered mice that overproduced a “mutant” type of the human amyloid-beta protein precursor gene.

They observe that in a earlier study, they had examined the substance on mice that normally overproduced mouse amyloid-beta. Even though this study was successful, the group wished to test the substance on a human form of the gene to see if it was just as successful.

The mice had high levels of the amyloid-beta protein, which enhanced inflammation in the brain and triggered damaged to the hippocampus, leading to learning and memory problems.

To serve as a comparison, the scientists examined a random antisense substance on healthy wild mice. Around half of the genetically engineered mice obtained the same antisense compound, while the other half got OL-1.

All mice were then subject to a set of studies that calculated learning, memory and appropriate behavior – like as identifying an object, discovering an unfamiliar location and discovering their way through a maze.

The group identified that the genetically engineered mice who obtained OL-1 exhibited enhanced learning and memory, in comparison with the genetically engineered mice that got the random antisense compound.

On contrasting the outcomes of OL-1 in genetically engineered mice and the random antisense substance in wild mice, the scientists identified no variations in learning and memory.

In addition, the scientists examined different injection sites of OL-1 on the mice, like as through the CNS so it entered the brain directly, and via a tail vein so it distributed the bloodstream. Nevertheless, they identified that injection site had no influence on outcomes.

Leaving comments on the research outcomes, Farr says:

“Our outcomes strengthen the significance of amyloid-beta protein in the Alzheimer’s disease process. They recommend that an antisense that targets the precursor to amyloid-beta protein is a possible treatment to explore to reversing symptoms of Alzheimer’s disease.”