Drug successfully reverses effects of Alzheimer's in rats

Drug successfully reverses effects of Alzheimer's in rats

A new study indicates that a drug may represent a novel therapeutic target for Alzheimer's disease after researchers used it to treat the disease in rats.

At present, the US Food and Drug Administration (FDA) have approved five medications to treat Alzheimer's disease. However, while these only mask the symptoms of Alzheimer's, the researchers were able to treat the disease itself in rats using a chemical called IRL-1620.

They found that the drug improved memory, prevented oxidative stress and enhanced neurovascular modeling in rats that had demonstrated impaired learning and increased oxidative stress caused by the disease.

"We used the novel approach of stimulating the endothelin B receptors by intravenous injection of IRL-1620 to prevent and repair the damage to the brain caused by Alzheimer's disease," reports study co-author Seema Briyal, a senior scientist and adjunct assistant professor at Midwestern University in Downers Grove, IL.

Endothelin B (ETB) receptors have previously been identified by researchers as important in brain development, and stimulation of these receptors has been shown to provide protection to the nervous system.

Alzheimer's disease is the most common cause of progressive dementia, a group of symptoms that impair brain function. An estimated 5.3 million Americans currently have Alzheimer's. According to the Alzheimer's Association, every 67 seconds, someone in the US develops the disease.

The condition is also one of the leading causes of death in the US, with the Alzheimer's Association estimating that 700,000 people will die with the disease over the course of 2015.

Memory deficit improved and oxidative stress reduced in rats with Alzheimer's

For the study, the researchers injected rats with Alzheimer's disease with IRL-1620, a drug known to bind to ETB receptors and observed its effects on spatial memory, oxidative stress and the expression of certain proteins in the brain.

The researchers found that the drug improved memory deficit in the rats by 50-60% and reduced oxidative stress by 45-50%.

"We also found that treatment with IRL-1620 enhanced certain recovery processes within the [Alzheimer's disease]-damaged brain, resulting in more new blood vessels and neuronal cells," Briyal adds. "This indicates reparative processes occurring in the damaged brain."

According to the researchers, this study is the first to demonstrate that intravenous injection of IRL-1620 can reverse the neurological effects of Alzheimer's disease in an animal model. Only time will tell if these results translate to humans with the chronic debilitating condition.

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