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Archive for June, 2007

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New Gene Therapy, Drug, Bring Hope

Friday, June 29th, 2007

The world has come a long way in learning and, treating Parkinson’s Disease (PD). Two studies published Thursday offer new hope for those affected by PD. One focuses on gene therapy to treat the symptoms of PD, another investigates a drug that could stop PD in its tracks; both treatments have limited testing with very small control groups, but nonetheless, a milestone in the treatment of PD. 

Gene therapy is an emerging treatment that has gained great attention with researchers and scientists. The gene therapy procedure that was announced on Thursday uses a harmless virus to carry a new gene into the brain. The idea behind gene therapy is to replace faulty genes or augment the activity of beneficial genes. The procedure had no ill effects and appeared to reduce symptoms. Dr. Michael Kaplitt a doctor at New York-Presbyterian Hospital and Weill Cornell Medical Center said, “These exciting results need to be validated in a larger trial, but we believe this is a milestone — not only for the treatment of Parkinson’s disease, but for the use of gene-based therapies against neurological conditions generally.”

In another study, released on Thursday a Harvard Medical group designed a drug that can protect the neurons damaged in PD, meaning, they may be able to halt the progression of PD right in its tracks. The drug could possibly, “protect neurons from cell death,” Alesksey Kazantsev who led the study, said in a telephone interview. They have tested their drug in lab dishes and fruit flies, which can be engineered to develop a condition highly similar to Parkinson’s in humans.

These treatments still need greater testing, but the direction research and technology is going points to a time when those suffering from Parkinson’s Disease, both patient and family, can find hope and assurance in a cure.

To read the quoted article, please click here

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Allergies Linked To Parkinson’s Disease

Monday, June 25th, 2007

Researchers from Mayo Clinic have discovered that allergic rhinitis is associated with the development of Parkinson’s disease later in life. Findings will be published in the Aug. 8 issue of the journal Neurology.

“The association with Parkinson’s disease is increased to almost three times that of someone who does not have allergic rhinitis,” says James Bower, M.D., Mayo Clinic neurologist and lead study investigator. “That’s actually a pretty high elevation.”

Previous studies had shown that people who regularly take nonsteroidal anti-inflammatory drugs, such as ibuprofen, are less likely to develop Parkinson’s disease. These results prompted the Mayo Clinic investigators to look further into the links between diseases characterized by inflammation and Parkinson’s. They studied 196 people who developed Parkinson’s disease, matched with people of similar age and gender who did not develop Parkinson’s. The study was conducted in Olmsted County, Minn., home of Mayo Clinic, over a 20-year period.

The researchers examined these groups to determine if those who developed Parkinson’s disease had more inflammatory diseases. They found that those with allergic rhinitis were 2.9 times more likely to develop Parkinson’s. They did not find a similar association between inflammatory diseases such as lupus, rheumatoid arthritis, pernicious anemia or vitiligo and Parkinson’s disease. The researchers hypothesize that they may not have found significant links between these diseases and Parkinson’s disease due to the relatively small number of those in the population who have these diseases, and thus the small number with these diseases in their population sample study. They also did not find the same association with Parkinson’s disease in patients with asthma that they discovered in those with allergic rhinitis.

Dr. Bower says that this study did not examine patients’ types of allergies or when they developed allergies.

The investigators theorize that a tendency toward inflammation is the key link between the diseases.

“People with allergic rhinitis mount an immune response with their allergies, so they may be more likely to mount an immune response in the brain as well, which would produce inflammation,” Dr. Bower says. “The inflammation produced may release certain chemicals in the brain and inadvertently kill brain cells, as we see in Parkinson’s.”

Dr. Bower explains that this study does not prove that allergies cause Parkinson’s disease; instead, it points to an association between the two diseases. He advises that allergy patients can do little to reduce the potential risk for Parkinson’s.

“I wouldn’t worry if you have allergies,” he says. “Treat the allergy symptoms you have to alleviate them at the time. At this point, we have no good evidence that this treatment will protect you from possibly developing Parkinson’s disease later.”

Dr. Bower and colleagues hope, however, that the clues in this study may give scientists a strong hint about inflammation’s role in Parkinson’s.

“This is exciting, because we may be able to develop medications to block the inflammation,” he says.

Parkinson’s is a complex disease, says Dr. Bower, because many factors can contribute to its development and its causes can differ. The complexity can be compared to heart attacks, which can be caused by hypertension, high cholesterol or smoking, among other factors. Thus, allergic rhinitis would now be considered one among many possible risk factors for development of Parkinson’s disease.

Parkinson’s disease affects nerve cells (neurons) in the part of the brain that controls muscle movement. People with Parkinson’s disease often experience trembling, muscle rigidity, difficulty walking, and problems with balance and coordination. These symptoms generally develop after age 50, although the disease also affects a small percentage of younger people. The normal lifetime risk to develop Parkinson’s disease for men and women combined is 1.7 percent.

Posted in General, News, Research | No Comments »

Drug Slows And May Halt Parkinson’s Disease

Sunday, June 24th, 2007

Northwestern University researchers have discovered a drug that slows – and may even halt – the progression of Parkinson’s disease. The drug rejuvenates aging dopamine cells, whose death in the brain causes the symptoms of this devastating and widespread disease.

D. James Surmeier, the Nathan Smith Davis Professor and chair of physiology at Northwestern University’s Feinberg School of Medicine, and his team of researchers have found that isradipine, a drug widely used for hypertension and stroke, restores stressed-out dopamine neurons to their vigorous younger selves. The study is described in a feature article in the international journal Nature, which was published on-line June 10.

Dopamine is a critical chemical messenger in the brain that affects a person’s ability to direct his movements. In Parkinson’s disease, the neurons that release dopamine die, causing movement to become more and more difficult.

Ultimately, a person loses the ability to walk, talk or pick up a glass of water. The illness is the second most common neurodegenenerative disease in the country, affecting about 1 million people. The incidence of Parkinson’s disease increases with age, soaring after age 60.

“Our hope is that this drug will protect dopamine neurons, so that if you began taking it early enough, you won’t get Parkinson’s disease, even if you were at risk. ” said Surmeier, who heads the Morris K. Udall Center of Excellence for Parkinson’s Disease Research at Northwestern. “It would be like taking a baby aspirin everyday to protect your heart.”

Isradipine may also significantly benefit people who already have Parkinson’s disease. In animal models of the disease, Surmeier’s team found the drug protected dopamine neurons from toxins that would normally kill them by restoring the neurons to a younger state in which they are less vulnerable.

The principal therapy for Parkinson’s disease patients currently is L-DOPA, which is converted in the brain to dopamine. Although L-DOPA relieves many symptoms of the disease in its early stages, the drug becomes less effective over time. As the disease progresses, higher doses of L-DOPA are required to help patients, leading to unwanted side-effects that include involuntary movements. The hope is that by slowing the death of dopamine neurons, isradipine could significantly extend the time in which L-DOPA works effectively.

“If we could double or triple the therapeutic window for L-DOPA, it would be a huge advance,” Surmeier said.

The work by Surmeier’s group is particularly exciting because nothing is known to prevent or slow the progression of Parkinson’s disease.

“There has not been a major advance in the pharmacological management of Parkinson’s disease for 30 years,” Surmeier said.

Surmeier, who has researched Parkinson’s disease for 20 years, had long been frustrated because it wasn’t known how or why dopamine cells die in the disease. “It didn’t seem like we were making much progress in spite of intense study on several fronts,” he said.

Because he’s a physiologist, Surmeier decided to investigate whether the electrical activity of dopamine neurons might provide a clue to their vulnerability. All neurons in the brain use electrical signals to do their job, much like digital computers.

First, Surmeier observed that dopamine neurons are non-stop workers called pacemakers. They generate regular electrical signals seven days a week, 24 hours a day, just like pacemaker cells in the heart. This was already known. But then he probed more deeply and discovered something very strange about these dopamine neurons.

Most pacemaking neurons use sodium ions (like those found in table salt) to produce electrical signals. But Surmeier found that adult dopamine neurons use calcium instead.

Sodium is a mild mannered ion that does its job without causing a whit of trouble to the cell. Calcium ions, however, are wild and rambunctious. Remember when Marlon Brando rode into town with his motorcycle gang in “The Wild One”" Those guys were like calcium ions.

“The reliance upon calcium was a red flag to us,” Surmeier said. Calcium ions need to be chaperoned by the cell almost as soon as they enter to keep them from causing trouble, he noted. The cell has to sequester them or keep pumping them out. This takes a lot of energy.

“It’s a little like having a room full of two year olds you have to watch like a hawk so they don’t get into trouble,” Surmeier said. “That’s really going to stress you.” With three boys under age eleven, he can relate to the stressed dopamine neuron.

Surmeier theorized that the non-stop stress on the dopamine neurons explains why they are more vulnerable to toxins and die at a more rapid rate as we age.

But these findings still didn’t offer him a new therapy.

Then, serendipity struck when he was working on a different problem. He discovered that young dopamine neurons and adult ones have an entirely different way of operating.

When the neurons are young, Surmeier found they actually use sodium ions to do their work. But as the neurons age, they become more and more dependent on the troublesome calcium and stop using sodium. This calcium dependence – and the stress it causes the neurons – is what makes them more vulnerable to death.

What would happen, Surmeier wondered, if he simply blocked the calcium’s route into the adult neuron cells” Would the neurons revert to their youthful behavior and start using sodium again”

“The cells had put away their old childhood tools in the closet. The question was if we stopped them from behaving like adults would they go into the closet and get them out again”" Surmeier asked. “Sure enough, they did.”

When he gave the mice isradipine, it blocked the calcium from entering the dopamine neuron. At first, the dopamine neurons became silent. But within a few hours, they had reverted to their childhood ways, once again using sodium to get their work done.

“This lowers the cells’ stress level and makes them much more resistant to any other insult that’s going to come along down the road. They start acting like they’re youngsters again,” Surmeier said.

The next step will be launching a clinical study.

“This animal study suggests that calcium channel blockers, drugs currently used to reduce blood pressure, might someday be used to slow the steady progression of Parkinson’s disease,” said Walter J. Koroshetz, M.D., deputy director of the NINDS.

Posted in General, News, Prevention, Research | No Comments »

Gene Therapy For Parkinson’s Disease

Friday, June 22nd, 2007

Injection of genetic information directly into the brain cells of patients (gene therapy) with neurodegenerative conditions such as Parkinson’s disease could safely alleviate symptoms of these conditions, conclude authors of an Article published in this week’s edition of The Lancet.

However an accompanying comment questions the advantages of gene therapy over deep-brain stimulation, a current method for treating Parkinson’s disease.

Professor Matthew During, Weill Medical College of Cornell University, New York, USA, and colleagues did a safety and tolerability trial on 11 men and one woman, average age 58 years. The patients were divided into groups of four and given low, medium, or high dose, injections of the glutamic acid decarboxylase (GAD) gene, with associated adeno-associated virus (AAV). The injections were given into the subthalamic nucleus of the brain, and all took place at the Weill Medical College of Cornell University/New York Presbyterian Hospital, USA.

All patients survived the surgery and had no side effects related to gene therapy. Substantial improvements in movement were seen within three months of surgery in the side of the body opposite to that of the brain where injections were given, and continued until 12 months after surgery-the endpoint of the trial. Improvements in motor scores were also seen in both the “on” state (when subjects were on standard medication, and typically not improved with other surgical approaches), as well as the “off” state despite the gene therapy being given in only one hemisphere.

Brain scans also showed reductions in metabolism in the ipsilateral thalamus (IT), similar to reductions which occur after other successful surgery for Parkinson’s disease. The study also showed a correlation between improved clinical motor scores and brain metabolism in the supplementary motor area, again similar to findings reported after surgery of patients with Parkinson’s disease.

The authors also point out that the gene therapy approach has advantages over the currently used deep-brain stimulation method. They say: “The absence of indwelling hardware [for gene therapy] reduces the risk of infection, and some patients with Parkinson’s disease simply prefer not to have the implanted device.” They add that frequent hospital visits would not be necessary for the gene therapy approach.

The authors conclude: “Our results show that AAV-mediated gene transfer can be done safely in the human brain, with no evidence of substantial toxic effects or adverse events in the perioperative period and for at least one year after treatment.”

In the accompanying Comment, Dr Jon Stoessl, Pacific Parkinson’s Research Centre, University of British Columbia, Canada, asks: “Apart from the avoidance of stimulator adjustments and potential hardware problems, what is the real advantage of this approach compared with deep-brain stimulation of the subthalmic nucleus?”

He concludes: “During and colleagues have taken a proactive approach to the treatment of neurodegenerative disease, and should be congratulated for their circumspection in the description of the potential implications of their findings. They made an important step in showing proof of principle, but much work should be done before neurologists and neuroscientists will regard this therapy as an effective approach.”

Posted in General, Research | No Comments »

New Tests, Treatments Close in on Alzheimer’s

Monday, June 18th, 2007

Doctors may soon have new tests to detect Alzheimer’s early on, as well as better medications to help treat the mind-wasting disease, researchers say.A number of advances against the disease were highlighted Monday at the Alzheimer’s Association’s International Conference on Prevention of Dementia in Washington, D.C.

In one presentation, researchers reported that a new test may spot Alzheimer’s early. And as effective therapies become available, earlier diagnosis will be key, experts say.

“Alzheimer’s disease is very difficult to diagnose when it is in its early stages,” said lead researcher Geert De Meyer, a senior biostatistician at Innogenetics in Gent, Belgium. “That’s a pity because therapy might be most effective when it is applied in an early stage.”

In the study, De Meyer’s team tested a new diagnostic test, called INNO-BIA, that detects and measures the amount of various forms of amyloid-beta protein in blood. A buildup of amyloid-beta in the brain is a hallmark, and possible cause, of Alzheimer’s.

The Belgian group tried the early detection test on blood samples taken from 556 people who had come to memory clinics with the early symptoms of dementia, including mild cognitive impairment.

According to the researchers, people at risk for Alzheimer’s had significantly different amyloid-beta levels in their blood compared with people who did not show risk of Alzheimer’s. For example, the ratio of amyloid-beta 1-42/amyloid-beta 40 was decreased by about 20 percent in patients at risk for Alzheimer’s, compared to those not at risk.

“This is really a first step,” De Meyer said. “The test could be used as a screening test or a risk-factor-determining test for Alzheimer’s disease that can be followed up with other tests.”

Another report focused on a phase II trial that tested LY450139, a drug being developed by Eli Lilly and Company. The medication is a potential treatment for Alzheimer’s because it inhibits an enzyme, known as gamma-secretase, which contributes to the formation of amyloid-beta.

The trial was led by Dr. Eric Siemers, medical director of the Eli Lilly Alzheimer’s Disease Team in Indianapolis. Siemers and his colleagues randomly assigned 51 patients with mild to moderate Alzheimer’s to either 100 milligrams or 140 milligrams of the drug for six to 12 weeks.

The result: Levels of amyloid-beta 1-40 were reduced by 58 percent for the 100 milligram group and by 64 percent for the 140 milligram group.

However, no differences were seen in patients’ cognitive function. But Siemers isnt disheartened by that outcome, he said, since “this was too short of a period to see a disease-modifying effect.”

“This is the most robust effect of amyloid-beta in blood of any drug that is currently under development,” he added. “The drug was safe, but we found some things that we will continue to monitor as we go into phase III studies, which will start early next year.”

A third study presented Monday tackled Alzheimer’s disease from a whole different angle. Experts know that glucose is the primary energy source for brain cells. However, in people with Alzheimer’s, scientists have now discovered that a dramatic dip in glucose use in certain brain areas starts 10 to 20 years before any symptoms of Alzheimer’s appear.

Deprived of their primary energy source, these stricken neurons suffer irreparable damage.

“This is a very novel approach to the treatment of Alzheimer’s disease,” said lead researcher Lauren Costantini, vice president for clinical development at Accera, in Broomfield, Colo. “The problem that we are focusing on is reduced brain glucose metabolism that has been shown to be an early event in Alzheimer’s disease.”

To replace this loss, scientists at Accera have developed a milkshake-like drug called AC-1202 (Ketasyn) that provides glucose-deprived neurons with an alternative energy source, known as ketone bodies. The researchers believe that increasing the availability of ketone bodies will improve memory problems and other functional losses that occur with Alzheimer’s.

Costantini’s team found that, after 45 days, people who took AC-1202 had statistically significant improvement in cognition compared with people taking a placebo. The best response was seen among people who did not have the E4 variant of the apolipoprotein gene (ApoE4), which occurs in half of all Alzheimer’s patients.

Those who continued to take the drug for nine months had very little disease progression, especially among the people without the E4 variant, Costantini reported.

“We see this as a potential co-therapy with other strategies,” Costantini said.

Posted in General, Research, Treatment Options | No Comments »

Rob Peppers Changes Forecast for Own Future

Friday, June 8th, 2007

For 19-years, viewers have counted on Rob Peppers to deliver the forecast on 13 News.

But for the past eight years, Rob’s shared more than the weather with all of us. He’s also shared his fight against Parkinson’s disease. The journey has led Rob to the decision that, for the sake of his health, he will leave an on-air position.

For Rob, his career has been a dream come true. He says he remembers as a child listening to the radio and being so disappointed in hearing a snow storm was going to miss his hometown of Salina. That passion continued into college and his first job at a local station in Salina. He recalls doing those first forecasts sticking magnets to a board and taping an hour in advance.

In 1988, Rob hit what he considered the big time – a job at WIBW-TV. Former Chief Meteorologist Dave Relihan recalls that Rob blew everyone away his first time on the air. He says rather than first-time nerves or stumbles, Rob was perfect, “and he’s been pretty much perfect his entire career.”

It all seemed perfect until 1995, when, at age 29, Rob noticed a twitching in his finger during a softball game. It led to a life-changing diagnosis of Parkinson’s disease. Still, it wasn’t a diagnosis Rob shared until 1999, when the symptoms became too much to hide.

Rob says he tried to hide it at first because he didn’t know how people would react. He says TV is known as a “pretty people’s” business, and he was afraid that if people saw something was wrong, they would change the channel. Instead, Rob says he got the opposite reaction with an outpouring of support from the public.

That support was never more important to Rob than in March of 2002. Rob underwent surgery to receive deep brain stimulation. Devices implanted in his chest connect to electrodes in the brain. The impulses help control his Parkinsons symptoms. Rob allowed cameras into his doctor appointments and the operating room.

Rob says it wasn’t a conscious decision to do it on TV or do it in private. He says he merely wanted people to see it’s an awful disease that does terrible things to people, but that there was also hope.

Rob says, in a lot of ways, the surgery has given him his life back. But as life goes on, so, too, does his disease. Rob says the surgery was more or less a stop-gap measure, not a cure.

“We still need a cure,” he says.

Over the last six months to a year, Rob says his symptoms have steadily gotten worse. He says he has some trouble walking at times and he’s finding he has more trouble with situations he normally wouldn’t at work.

That includes being on camera. When the red light goes on, 10- to 20-thousand people are watching, and that can be stressful.

Rob says if you watch, the video tells the story. He says anytime a camera is on, it creates a stressful situation for him, and he can’t control the shaking Parkinsons causes. Parkinsons and stress, he says, is a bad combination, and being in severe weather season when lives are at stake, he says he feels a responsibility to hand hand it off to those better capable of handling the situation.

For the sake of his health, Rob will step off-camera and go to work full-time in WIBW-TV’s business office. But you’ll still see him from time to time, filling in for Jeremy Goodwin, Candice Sorensen and Drew Switzer, and staying in the thick of the action.

“I’ll still be able to chase storms which is big for me!” Rob says.

Rob says his new position will lower his stress and give him an eight to four schedule, so he can get a good night’s sleep. After eight years of fighting Parkinsons in the public eye, Rob says he’ll sign off knowing how much support is out there.

“I wish I could go to every person who has sent a card or a letter,” he says. “It’s amazing the support I’ve received. If I could say one thing it would be thank you for all you’ve done.”

The Future of Parkinson’s Treatment and Research
Twelve years, lots of pills and one major surgery since his diagnosis with Parkinson’s Disease, Rob Peppers refuses to give up hope. He says while it is a frustrating disease in many ways, he believes the overall picture down the road is bright.

Experts agree.

“There is a lot of fear,” says Cotton-O’Neil Neurologist Dr. Ernie Swanson. “But for the vast majority of people, there are a lot of options, those options are improving year by year and the long-term prognosis is good.”

Swanson says some of the biggest advances are in new medications. The neurotransmitter dopamine is reduced in Parkinsons patients. The newer meds act on the brain in a way that more closely mimics what dopamine would do naturally. Swanson says the more that can be done, “the more we can delay the process and reduce side effects people have.”

The other challenge comes in diagnosing Parkinsons. Swanson says new tests have been developed to help doctors catch it earlier. He says many times, when patients are diagnosed, there are already changes in the brain. He says that means doctors are seeing a process that’s already been going on for five or six years. He says the earlier Parkinsons can be diagnosed, the earlier treatment can start treatment and the better patients will do.

Of course, being aware of a disease is the first step in battling it. On that front, Swanson agrees Rob has made a difference.

“His position, his recognition, has meant a lot to a lot of people both with Parkinsons disease and without it,” he said. “He’s had a huge impact on people being aware of Parkinsons in Kansas.”

But Rob says it’s the people who’ve had the bigger impact on him.

“I’m just me trying to live my life,” Rob says. “A lot of people are suffering a lot more than me. I feel I represent them when I’m on camera.”

Posted in General | No Comments »

Faust Pharmaceuticals’ Phase IIa Results For Parkinson’s Disease Showed Good Tolerance And Combination Of Therapeutic Effects

Thursday, June 7th, 2007

Faust Pharmaceuticals S.A., a clinical stage product company specializing in the discovery and development of drugs for diseases of the nervous system, today announced that the Phase IIa clinical trial results of its small molecule glutamate release inhibitor, FP0011, are being presented at the Movement Disorder Society (MDS)’s 11th International Congress of Parkinson’s Disease and Movement Disorders, taking place this week in Istanbul, Turkey. The poster, presented by the study’s Principal Investigator, Olivier Rascol, M.D., of University Hospital, Toulouse, has been selected for presentation at the Highlights of Posters session during the conference.

In the trial, FP0011 was well tolerated and improved Parkinsonian symptoms as measured by the Unified Parkinson’s Disease Rating Scale (UPDRS), as well as motor fluctuations as measured by patient diaries. The compound had positive effects in three critical areas: “core” Parkinsonian motor symptoms (such as tremor, rigidity and akinesia), axial symptoms not sensitive to L-dopa and other commonly-prescribed dopaminergic drugs (such as disturbance of posture, balance and gait), and dyskinesia (i.e. the jerky uncontrolled movements that result as a side effect of long term L-dopa therapy).

The Phase IIa trial was conducted according to an innovative “n of 1″ trial design in which a small population (n=8) of mid-to-late stage Parkinsonian patients with L-dopa-induced motor complications were administered FP0011 or placebo over 4 cross-over periods on a randomized, blinded basis.

Professor Rascol, Dr. Joaquim Ferreira (Lisbon), and Dr. Lucette Lacomblez (Paris), were principal investigators in this Phase II trial. The “n of 1″ trial design was previously used by Dr. Ferreira to confirm that amantadine, originally developed as an antiviral and now commonly used to address side effects of L-dopa therapy, could help Parkinson’s patients.

“The differentiated profile observed in this Phase II trial is interesting and intriguing as there are currently no other drugs with this combination of therapeutic effects,” said Professor Rascol. “Particularly if the therapeutic effect on non-levodopa sensitive symptoms can be confirmed in the Phase IIb and subsequent trials, the compound would address a very important unmet medical need for all mid-to-late stage patients developing postural disturbances, and could represent a significant advance in approaches to Parkinson’s disease.”

Also being presented at the conference is a poster on the results of FP0011 in a MPTP macaque monkey model of Parkinson’s disease, by Dr. Jonathan Brotchie, CEO of Atuka Ltd. of Toronto, Canada. In this trial, monkeys that have developed dyskinesia from the administration of L-dopa to treat Parkinsonian symptoms from the neurotoxin, MPTP, were administered FP0011. FP0011 reduced the severity of L-dopa-induced dyskinesia while extending the duration of the anti-Parkinsonian action of L-dopa.

“Unlike other drugs on the market that increase the duration of L-dopa action, FP0011 did not exacerbate the problem of dyskinesia,” said Dr. Brotchie. “If these effects were seen in patients, then over the course of a day such an action could significantly enhance the quality of life of people with advanced Parkinson’s disease.”

Commenting on these presentations, Thomas Seoh, CEO of Faust noted that: “These mutually supportive data in the Phase IIa trial and the MPTP monkey trial presented at this conference strongly support the further clinical development of FP0011 as an adjunctive therapy to L-dopa in patients with established motor complications. We look forward to confirming and extending these results in larger trials for Parkinson’s patients. Ultimately, we hope to demonstrate that FP0011 can be a potent, safe glutamate release inhibitor that could have a role in other neurological diseases and conditions where excess glutamate has been implicated, such as Alzheimer’s disease, ALS, Huntington’s disease, multiple sclerosis and neuropathy.”

About Faust Pharmaceuticals

Faust Pharmaceuticals is a clinical stage products company specializing in the discovery and development of drugs for diseases of the nervous system. The company’s lead compound, FP0011, is a small molecule glutamate inhibitor in Phase II for Parkinson’s disease and ALS. A second compound, FP0023, is a fetal gene activating utrophin inducer in preparation for Phase I/II for Duchenne Muscular Dystrophy. The company additionally has pre-clinical programs on targets such as mGluR (metabotropic glutamate receptor), as well as a proprietary drug discovery platform targeting GPCRs (G-Protein Coupled Receptors).

http://www.faustpharma.com/

Posted in Clinical Trial, General, Research | No Comments »

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