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Scientists are working on a new drugy therapy that would decrease brain inflammation by binding to and decreasing cytokines! See below......
For full text of article please see:
http://www.foxnews.com/health/2012/...ug-could-treat-alzheimer-ms-and-brain-injury/
Alzheimer’s, Parkinson’s disease, multiple sclerosis and traumatic brain injury are four neurodegenerative disorders with very different – and very devastating – effects on the brain and daily life.
While there are multiple treatments and therapies aimed at fighting each of these conditions separately, a team of researchers from Northwestern University Feinberg School of Medicine have developed a new “one-size-fits-all” therapy drug that could potentially treat all of them.
The drug’s trick lies in reducing a particular type of inflammation in the brain known as neuroinflammation. This brain response has become increasingly considered a common denominator for many neurological disorders, as well as playing a major role in brain injuries. To decrease inflammation, the drug developed at Northwestern binds to and decreases a molecule known as cytokine, which is released in large quantities during the neuroinflammatory response.
“We faced two main challenges,” Dr. Martin Watterson, a professor of molecular pharmacology and biological chemistry at the Feinberg School, as well as the lead developer of the drug, told FoxNews.com. “Come up with something to tone down the inflammatory response and do it with some selectivity [so that the immune response would not be toned down as well]. “We wanted to have a small molecule taken by mouth once or twice a day that would be relatively safe and get into the brain.”
Published in the Journal of Neuroscience, the study showed the success of the drug in preventing progression of Alzheimer’s in mice that were genetically engineered to develop the disease. When the mice were evaluated 11 months after being administered the drug, their inflammation had decreased, and their brain synapses were functioning normally.
While the results are encouraging, Watterson said there’s still some ways to go.
“The design, the synthesis and testing [of the drug] took less than a year,” Watterson added. “In drug development, that’s called a hit. It’s like a bite when you’re fishing, it’s significant, but you still have to reel in the fish… You have to take the hit and improve on it to get a lead compound which has better activity in vivo and does not have bad activity.”
For full text of article please see:
http://www.foxnews.com/health/2012/...ug-could-treat-alzheimer-ms-and-brain-injury/
Alzheimer’s, Parkinson’s disease, multiple sclerosis and traumatic brain injury are four neurodegenerative disorders with very different – and very devastating – effects on the brain and daily life.
While there are multiple treatments and therapies aimed at fighting each of these conditions separately, a team of researchers from Northwestern University Feinberg School of Medicine have developed a new “one-size-fits-all” therapy drug that could potentially treat all of them.
The drug’s trick lies in reducing a particular type of inflammation in the brain known as neuroinflammation. This brain response has become increasingly considered a common denominator for many neurological disorders, as well as playing a major role in brain injuries. To decrease inflammation, the drug developed at Northwestern binds to and decreases a molecule known as cytokine, which is released in large quantities during the neuroinflammatory response.
“We faced two main challenges,” Dr. Martin Watterson, a professor of molecular pharmacology and biological chemistry at the Feinberg School, as well as the lead developer of the drug, told FoxNews.com. “Come up with something to tone down the inflammatory response and do it with some selectivity [so that the immune response would not be toned down as well]. “We wanted to have a small molecule taken by mouth once or twice a day that would be relatively safe and get into the brain.”
Published in the Journal of Neuroscience, the study showed the success of the drug in preventing progression of Alzheimer’s in mice that were genetically engineered to develop the disease. When the mice were evaluated 11 months after being administered the drug, their inflammation had decreased, and their brain synapses were functioning normally.
While the results are encouraging, Watterson said there’s still some ways to go.
“The design, the synthesis and testing [of the drug] took less than a year,” Watterson added. “In drug development, that’s called a hit. It’s like a bite when you’re fishing, it’s significant, but you still have to reel in the fish… You have to take the hit and improve on it to get a lead compound which has better activity in vivo and does not have bad activity.”
