Priscilla Tasker
Issue date: 3/20/07 Section: News
Neurodegenerative diseases such as Alzheimer's disease, multiple sclerosis, Parkinson's disease and others affect more than 20 million people worldwide.
Researchers at Northeastern Ohio Universities College of Medicine and Pharmacy in Rootstown, have been conducting research to develop a drug that could stop the processes that cause such diseases. The focus of the research is a molecule called NGP1-01, which has the potential to treat several factors that result in the deterioration of neurons in the brain, said Dr. Neels Van der Schyf, founding chair of NEOUCOM and professor at Kent State.
"Each individual has 80 to 90,000 dopaminergic neurons," Van der Schyf said. "Now that sounds like a lot, but you reach your peak in your early 20s. After that they start to die down one by one."
Dopaminergic neurons control brain functions including voluntary movement and behaviors associated with stress, mood and addiction, according to the National Center for Biotechnology Information Web site. Loss of this type of neuron is characteristic of Parkinson's disease.
A person may lose up to 80 percent of those neurons and still operate normally, never knowing that something is happening. Symptoms of a neurodegenerative disease would begin to surface when the neurons are depleted to about 20 percent, Van der Schyf said.
The theory behind the drug research is that the neurodegeneration can be slowed down before reaching that 20 percent range.
"Arguably if we could catch an individual with 30 percent of the (neurons) still intact we could probably prevent the neurodegeneration and have them live out a normal life," Van der Schyf said.
NGP1-01 has the potential to treat certain causes of neurodegeneration because of its ability to cross the blood-brain barrier. This means that the molecule is able to access cells in the brain, which is a rare discovery, Van der Schyf said.
The molecule's mechanism as a calcium-channel blocker balances the calcium influx in the brain cells that leads to the deterioration of the neurons, he said. It also has the ability to weaken or lessen excitotoxicity in the brain. Excitotoxicity refers to an excessive release of the chemical that transports messages from cell to cell, according to the Harvard Center for Neurodegeneration and Repair.
"If we have a mechanism by where we could very effectively and accurately diagnose an individual's propensity to develop Parkinson's, I believe we that have the tools to prevent that," Van der Schyf said, "Here's the dilemma, you may argue that OK, it's great to give a drug to everybody because we already know that the drug's going to prevent (it), but you don't know what the drug's going to do elsewhere. It may cause heart problems, it may do all kinds of things, which is why we cannot do that ethically."
In 2004, Vioxx, an inflammatory medication produced by Merck Inc., was pulled from the market because a study had found a higher rate of heart attack and stroke in patients who were on the drug.
"It was never discovered when they went to market, so we need to be extremely careful when giving any kind of molecule to a group of people," Van der Schyf said.
The Food and Drug Administration has strict rules for developing and marketing new drugs, he said. On average it takes about 12 years of research and clinical trials before the FDA approves a drug, and additional post-marketing studies are required as well, according to the Alliance Pharmaceutical Corp. Web site.
NGP1-01 is still in the pre-clinical testing phase of drug development, and researchers are testing the affect of the molecule in mice.
About five of nearly 5,000 drugs enter clinical trials (human testing sequences), according to Alliance Pharmaceutical's Web site, but only one of the five drugs receives approval from the FDA.
NGP1-01 will probably never make it to market, Van der Schyf said, but the goal of the research is to open the doors to other discoveries in neuro-drug development.
Contact health trends and NEOUCOM reporter Priscilla Tasker at ptasker@kent.edu.
