Antisense Compound Developed to Reverse Symptoms of Alzheimer’s in Saint Louis University

Alzheimer’s disease (AD) is a condition wherein impairment in cognitive and memory functions becomes apparent in affected individuals. It is a progressive disorder and was known to have no definitive cure as of the moment.

AD is known to be caused by an accumulation of an abnormal protein, the human amyloid beta protein, in the brain, causing inflammation and oxidative stress on the parts of the brain where memory and cognitive functions are processed.

A recent biochemical engineering research in Saint Louis University explores the possibility of reversing the symptoms of AD in affected individuals and possibly treating the disease, making it another addition to several studies of biomedical science innovations. It was published in the May issue of the Journal of Alzheimer’s Disease.

The biochemical science research, led by Susan Farr, Ph.D., research professor of geriatrics at Saint Louis University, is the successor of a previous study in animal models which initially introduced an antisense compound which may be of therapeutic value in patients with Alzheimer’s Disease.

According to Farr, the molecular compound was able to restore memory, learning and appropriate behavior in mice models of Alzheimer’s Disease. Hence the compound, dubbed as antisense oligonucleotide (OL-1), proved to be a potential treatment to AD. An antisense is a molecule which binds to a compatible messenger RNA initiating a series of events which may eventually lead to a continuation or cessation of the production of a specific protein. In this case, the said antisense molecule (OL-1), was observed to significantly decrease the overexpression of the amyloid beta protein precursor. The latter is the protein said to be partly responsible for the accumulation of plaques in the brain leading to cognitive and memory impairment.

Although the compound was found to be effective in animal studies, it is yet to undergo clinical trials to establish its safety and therapeutic role in humans. Tests which include that for toxicity levels need to be done to be able to proceed to human clinical trials, Farr points out.

The study was carried out by comparing two groups of mice. The first group was genetically engineered to overproduce the abnormal amyloid protein. The second group, which is the wild strain, served as the control. Half of the genetically engineered mice received the antisense OL-1, half received a random antisense. All of the wild strains received random antisense.

A series of biochemical engineering tests were carried on to test the animals’ learning and memory skills. This includes going through mazes and introduction to an object or place that the animals have never been exposed to before.

The results showed that the genetically engineered mice which received OL-1 and the wild strain which received random antisense have had improved learning and memory. This is in comparison with the genetically engineered mice who received random antisense.

Further testing done by the team included the comparison of administration of the antisense whether directly through the central nervous system or through a venous route in the tail. They found no significant difference on learning and memory between the two routes.

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