Drug may treat MS, Alzheimer's and brain injury.

The Northwestern University Feinberg School of Medicine recently developed a new class drugs which is showing early promise to treat Parkinson's disease, Multiple Sclerosis, Alzheimer's disease, and traumatic brain injury by reducing inflammation in the brain.


The commercial development is on its way, this medicine is being developed by the same biotech company which has recently completed the first human phase clinical trial for this drug.


The drugs, currently known as MW151 and MW189, targets a particular type of brain inflammation that is a common denominator in MS, Parkinsons, Alzheimer, and also in traumatic brain injury and stroke.


With these recent discoveries, especially this, has raised scientist attention and they are coming to the conclusion that the idea of inflammation plays a very important role in progressive damage that is characterized in all of these chronic neurological diseases and brain injuries.


A pre-clinical study that was published July 24  stated that Northwestern's researchers report that when MW-151 is given to a mouse genetically engineered to develop Alzheimer's, it was noted to stop the full-blown diseases progression.


"This could become part of a collection of drugs you could use to prevent the development of Alzheimer's," said D. Martin Watterson, a professor of molecular pharmacology and biological chemistry at the Feinberg School, whose lab developed the drug.

In previous animal studies, the same drug reduced the neurological damage that is caused by closed-head traumatic brain injury and inhibited the development of a multiple sclerosis-like disease.


These drugs work by preventing the damaging overproduction of pro inflammatory cytokines.


When cytokines are overproduced, the synapses of the brain begin to misfire. Over the course of time the brains entire organization goes into chaos, and eventually the neurons lose their connection with each other and can die.

 "In Alzheimer's disease, many people now view the progression from mild cognitive impairment to full-blown Alzheimer's as an indication of malfunctioning synapses, the pathways that allow neurons to talk to each other," said Watterson, the John G. Searle Professor of Molecular Biology and Biochemistry. "And high levels of pro inflammatory cytokines can contribute to synaptic malfunction."

New Study

In the new study, a mouse model with Alzheimer's received MW151 three times a week at a six months age, right as the pro inflammatory cytokines begin to rise. At this stage, it is similar to when a human patient would begin to experience mild cognitive impairment.

These mice were evaluated five months from the time it received MW151, and researchers found that the cytokine levels in the mice receiving the drug were restored to normal levels and their synapses were functioning normally. However, the inflammatory cytokine levels on the mice which did not receive the drug was still abnormally high.

It was also noted: The mice which did not receive MW151 had misfiring synapses.

"The drug protected against the damage associated with learning and memory impairment,"Van Eldik noted. "Giving this drug before Alzheimer's memory changes are at a late stage may be a promising future approach to therapy."

Multiple Sclerosis Development (OnGoing)

In Multiple Sclerosis, the overproduction of the pro inflammatory cytokines damage the central nervous system and the brain.

When mice that were induced to develop an M.S.-like desease received MW151 orally,  the disease did not develop as severe.

"We inhibited the development of the disease," said William Karpus, the Marie A. Fleming Research Professor of Pathology at the Feinberg School. "Now we need to learn if the drug can prevent relapses of M.S."

This study is not yet finalized and the results are yet to be determined.

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