Drug successfully reverses the effects of Alzheimer's in rats, fully restoring memory function.
Adam Rifkin stashed this in Medicine
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 stresscaused 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.
Top Reddit comment:
This is one of the more promising basic science papers out in the past few years. The more we understand the pathophysiology of AD the better we can intervene with small molecules. It's only a matter of time - this has been the same story with every disease, and cancer is the best example.
This molecule binds to a receptor class called Endothelia B-type, which are thought to play a role in neuronal development. When activated with this agonist (agonists are molecules that bind to a receptor and activate it; as opposed to antagonist that bind to a receptor and block it like a decoy), the investigators noted new blood vessel formation and an increase in neuronal cell counts. These data are some of the most promising with respect to neuronal expansion in AD models.
Again it's just another piece of the puzzle, which is still in its infancy. Now that we know that this pathway is important in reversing the symptoms scientists will continue to refine small molecules that can intervene here
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