Summary:
A molecular compound (OL-1) made by Saint Louis University students was able to restore memory, learning, and behavior in mice with a mouse model of Alzheimer's. The compound was also able to get rid of inflammation in the parts of the brain responsible for memory and learning. It is a possible cure for humans. "OL-1 blocks the translation of RNA, which triggers a process that keeps excess amyloid beta protein from being produced". The excess amyloid beta protein could be partially responsible for Alzheimer's disease. In order for this to be useful in humans the compound needs to be able to stop the beta protien from being produced.
Relevance:
This Article is relevant because Alzheimer's very common and many people are effected and as of now there is no cure. With this product there is data to prove that the the major factor is the excess beta protein build up. From that discovery it can help scientists focus on what needs to be done in order to find a cure. Also the OL-1 is a very good step in the right direction because it has already been proven to get rid of some of the symptoms of Alzheimer's. In class we learned about the nervous system Alzheimer's is a very prominent disease that effects the brain.
Date: May 20th 2014
Link:http://www.sciencedaily.com/releases/2014/05/140520184640.htm
How would the compound be implanted in humans (pill, injection, etc)?
ReplyDeleteHow does the compound get rid of the inflammation in parts of the brain?
ReplyDeleteOlivia- They said it was a drug so my guess is that it would be a pill
ReplyDeleteJordan- this is and excerpt from the article that explains how the compound works: "Antisense is a strand of molecules that bind to messenger RNA, launching a cascade of cellular events that turns off a certain gene.
In this case, OL-1 blocks the translation of RNA, which triggers a process that keeps excess amyloid beta protein from being produced. The specific antisense significantly decreased the overexpression of a substance called amyloid beta protein precursor, which normalized the amount of amyloid beta protein in the body. Excess amyloid beta protein is believed to be partially responsible for the formation of plaque in the brain of patients who have Alzheimer's disease" (Saint Louis University Medical Center).