Now they want to know if a smell test can help determine if people with no symptoms eventually develop the disease.

“The analogy would be like diagnosing coronary artery disease before the heart attack,” says Dr. Kapil Sethi, director of the Movement Disorders Program at the Medical College of Georgia and a lead investigator the Parkinson’s Associated Risk Syndrome Study. “With Parkinson’s, we are dependent on the presence of motor symptoms like tremors, stiffness and slowness in order to diagnose it. By that time you have lost 50 to 60 percent of your dopaminergic cells, which make dopamine and are key to movement control. The question becomes, is there a window between when you had non-motor symptoms like loss of smell and when you begin to demonstrate clinical motor symptoms?”

Dr. Sethi and researchers at 17 other sites across the country will recruit 15,000 close relatives of Parkinson’s patients as part of the study, which is being led by the Institute for Neurodegenerative Disorders and the University of Pennsylvania.

“By testing those with a family history of the disease, we have an enriched population,” he says. “We already know that those people are more at risk. To enrich the sample even further, we’ll test their sense of smell. It’s not just the essence of a sense of smell that is different in these people. It’s a quantitative decrease in their ability to distinguish odors.”

Patients will be given the University of Pennsylvania’s Smell Identification Test, which tests for 40 common odors and has been used to detect the first signs of neurodegenerative disorders.

People with a normal sense of smell who take the test can usually identify around 35 odors correctly. Parkinson’s patients typically can only identify 20 or less.

The study will also help determine if the smell test can also predict who will get Parkinson’s.

“We believe that if you’re a person who is going to develop Parkinson’s, you’ll also score lower than others,” Dr. Sethi says.

Based on the results of the smell test, study participants will be divided into two groups – those with a normal sense of smell and those without. Both groups will undergo functional neuroimaging analyses at the Institute for Neurodegenerative Disorders in New Haven. Functional neuroimaging can identify changes in brain activity associated with Parkinson’s.

Both also will be clinically examined by a movement disorder specialist and followed for three to five years.

“We believe that a proportion of those who have the deteriorated sense of smell will develop Parkinson’s over the next two or three years,” Dr. Sethi says.

Study participants also will be asked about other common symptoms of the disease that may be present prior to the telltale motor symptoms. For example, people with Parkinson’s and other neurological diseases often suffer from a sleep disorder called REM Behavior Disorder, which causes them to act out their dreams.

“While most people are paralyzed when they dream so they can’t hurt themselves or others, people with Parkinson’s are not,” Dr. Sethi says. “They yell, scream and kick. No one knows why, but half of the people who have this sleep disorder will develop Parkinson’s or a similar disease.”

Questions about excessive daytime sleepiness and anxiety and constipation – other pre-symptoms of Parkinson’s – also will be asked.

“The goal is to give someone a degree of risk based on one or multiple factors,” Dr. Sethi says. “We don’t know specific numbers now, but hopefully, in the future, we will be able to tell people who have a deteriorated sense of smell and the sleep disorder specifically how much their risk goes up.”

The long-term goal, he says, is to develop prevention strategies once risk is established.

The Neurologix procedure delivers a gene (glutamic acid decarboxylase, or GAD) to the subthalamic nucleus of the brain, where it makes an inhibitory neurotransmitter called GABA that helps to quiet the abnormal brain activity that is correlated with motor deficits characterizing Parkinson’s disease. Results of a Phase 1 clinical study showed that the Neurologix gene transfer procedure was both well tolerated and resulted in improved motor function and brain metabolism for patients with advanced Parkinson’s disease over the course of the one-year study. Neurologix is currently preparing to initiate a Phase 2 study of its Parkinson’s disease treatment by early 2008, subject to final FDA consent to the study protocol.

“The FDA’s Fast Track Designation for this gene transfer procedure for Parkinson’s disease recognizes the need for new therapies for patients with advanced Parkinson’s disease who no longer receive adequate benefit from their drug therapies alone,” said John Mordock, President and Chief Executive Officer of Neurologix.

Under the FDA Modernization Act of 1997, Fast Track Designation may facilitate the development and expedite the review of a drug candidate that is intended for the treatment of a serious life-threatening condition and demonstrates the potential to address an unmet medical need for such a condition. Fast Track Designation will provide various means to expedite the development and review of the Neurologix gene transfer procedure for Parkinson’s disease, including the facilitation of meetings and other correspondence with FDA reviewers, consideration for priority review, and the ability to submit portions of a Biologics License Application (BLA) early for review as part of a “rolling” submission. The receipt of Fast Track Designation does not, however, assure the approval of any of Neurologix’s study protocols or the ultimate approval of any BLA that may be submitted by Neurologix to FDA for marketing approval.

About Neurologix

Neurologix, Inc. (NRGX.OB) is a clinical-stage biotechnology company dedicated to the discovery, development, and commercialization of life-altering gene transfer therapies for serious disorders of the brain and Central Nervous System (CNS). Neurologix’s therapeutic approach is built upon the groundbreaking research of its scientific founders and advisors, whose accomplishments have formed the foundation of gene therapy for neurological illnesses. Current company programs address such conditions as Parkinson’s disease, epilepsy and Huntington’s chorea, all of which are large markets not adequately served by current therapeutic options.

http://www.neurologix.net

Cautionary Statement Regarding Forward-looking Statements

This news release includes certain statements of the Company that may constitute “forward-looking statements” within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended, and which are made pursuant to the Private Securities Litigation Reform Act of 1995. These forward-looking statements and other information relating to the Company are based upon the beliefs of management and assumptions made by and information currently available to the Company. Forward-looking statements include statements concerning plans, objectives, goals, strategies, future events, or performance, as well as underlying assumptions and statements that are other than statements of historical fact. When used in this document, the words “expects,” “promises,” “anticipates,” “estimates,” “plans,” “intends,” “projects,” “predicts,” “believes,” “may” or “should,” and similar expressions, are intended to identify forward-looking statements. These statements reflect the current view of the Company’s management with respect to future events. Many factors could cause the actual results, performance or achievements of the Company to be materially different from any future results, performance or achievements that may be expressed or implied by such forward-looking statements, including, but not limited to, the following:

The Company is a development-stage company and has not generated any revenues. From inception through September 30, 2007, it incurred net losses and negative cash flows from operating activities of approximately $26.2 million and $20.3 million, respectively. Management believes that the Company will continue to incur net losses and cash flow deficiencies from operating activities for the foreseeable future. Because it may take years to develop, test and obtain regulatory approval for a gene-based therapy product before it can be sold, the Company likely will continue to incur significant losses for the foreseeable future. Accordingly, it may never be profitable and, if it does become profitable, it may be unable to sustain profitability.

In addition to the recently completed financing, in order to obtain the regulatory approvals necessary to commercialize its current or future product candidates, from time to time the Company will need to raise funds through public or private equity offerings, debt financings or additional corporate collaboration and licensing arrangements. Availability of financing depends upon a number of factors beyond the Company’s control, including market conditions and interest rates. The Company does not know whether additional financing will be available when needed, or if available, will be on acceptable or favorable terms to it or its stockholders.

The Company will need to conduct future clinical trials for treatment of Parkinson’s disease using the Company’s NLX technology. If the trials prove unsuccessful, future operations and the potential for profitability will be materially adversely affected and the business may not succeed.

There is no assurance as to when, or if, the Company will be able to successfully receive approval from the FDA on its Investigational New Drug Application to commence a Phase I safety trial for the treatment of epilepsy.

Other factors and assumptions not identified above could also cause the actual results to differ materially from those set forth in the forward-looking statements. Additional information regarding factors that could cause results to differ materially from management’s expectations is found in the section entitled “Risk Factors” in the Company’s 2006 Annual Report on Form 10-KSB. Although the Company believes these assumptions are reasonable, no assurance can be given that they will prove correct. Accordingly, you should not rely upon forward-looking statements as a prediction of actual results. Further, the Company undertakes no obligation to update forward-looking statements after the date they are made or to conform the statements to actual results or changes in the Company’s expectations.

“We are proud to have established this collaboration with Merck because their researchers have helped to define the therapeutic potential of targeting mGluR4 to treat Parkinson’s disease,” Vincent Mutel, CEO of Addex, said. “This is another important validation of our leadership in allosteric modulation.”

“Addex has made exceptional progress in the area of mGlu receptor allosteric modulation,” said Darryle D. Schoepp, Ph.D., senior vice president and franchise head, Neuroscience, at Merck Research Laboratories. “This partnership is key to us jointly establishing a leadership position in the promising area of mGluR4 receptor modulation for Parkinson’s disease. Merck scientists are excited to work with Addex to extrapolate the full value of this novel mechanism for a range of neuroscience disorders.”

Parkinson’s disease is a debilitating movement disorder. Current treatments focus on dopamine-replacement strategies, however most patients reach a stage where these treatments are no longer effective. There can also be debilitating side effects with current treatments and many patients limit doses so their symptoms are less cumbersome. The recent success of surgical approaches suggests that bypassing the dopamine system may provide a more effective treatment strategy. It is believed that selective activation of mGluR4 is one way to do this and could correct the circuitry that modulates motor excitability. This has the potential to provide significant palliative benefit in Parkinson’s disease.

Under the terms of the agreement, Addex will receive $3 million upfront and is eligible for up to $106.5 million in research, development and regulatory milestones for the first product developed for multiple indications. Additional milestones of up to $61 million would be payable if a second and third product is developed. Addex is eligible to receive undisclosed royalties on sales of any products resulting from this collaboration.

Addex and Merck will collaborate on preclinical development. Merck will be responsible for clinical development. Addex has an option to co-promote in certain European Union countries and will participate in the joint oversight committee for clinical development. Addex will host a webcast & teleconference (see below).

Targeting glutamate receptors

Like dopamine and serotonin, glutamate is a key neurotransmitter in the human brain, an important signaling molecule involved in control of multiple brain functions ranging from motor control to mood. Although marketed drugs modulate specific receptors involved in both the dopaminergic and serotinergic systems, it has been difficult to develop drugs that target specific G protein coupled receptors in the glutamatergic system.

Merck has been a pioneer in research on mGlu receptors and the metabotropic glutamatergic system for multiple indications. For example, research by Merck scientists provided the first evidence that mGluR4 activation has potential for treatment of Parkinson’s disease. However, a remaining challenge has been to make drug-like molecules that activate mGluR4 in a specific fashion. Addex is a pioneer in developing truly selective small molecule drug candidates targeting glutamate receptors and has previously disclosed programs targeting mGluR5 and mGluR2.

mGluR4 in Parkinson’s disease

Published research* shows that mGluR4 activators, like those in development at Addex, could work via two distinct mechanisms to alleviate symptoms of Parkinson’s disease and, potentially, even slow the progression of the disease: 1) mGluR4 activation triggers a compensatory mechanism that may spare or potentiate the use of dopamine receptor activators; 2) mGluR4 activation may have a neuroprotective effect that helps to preserve the brain’s dopaminergic neurons.

*Nature Reviews Neuroscience, Vol 6, Oct. 2005, pp 787-798

About Parkinson’s disease

Parkinson’s disease is a brain disorder. It occurs when certain nerve cells (neurons) in a part of the brain called the substantia nigra die or become impaired. Normally, these cells produce a signaling molecule (neurotransmitter) known as dopamine. Among other things, dopamine allows smooth, coordinated function of the body’s muscles and movement. When approximately 80 percent of the dopamine-producing cells are damaged, the symptoms of Parkinson’s disease appear.

Parkinson’s disease affects both men and women in almost equal numbers. It shows no social, ethnic, economic or geographic boundaries. In the United States, it is estimated that 60,000 new cases are diagnosed each year, joining the 1.5 million Americans who currently have Parkinson’s disease. While the condition usually develops after the age of 65, 15 percent of those diagnosed are under 50.

Most symptoms associated with Parkinson’s disease, like tremor, rigidity and slowness, are caused by a lack of dopamine. Marketed medicines help to ease the symptoms of Parkinson’s disease by either replacing or mimicking dopamine. Currently, no marketed products slow the disease progression. No marketed products work via non-dopaminergic mechanisms.

About Addex

Addex Pharmaceuticals discovers and develops allosteric modulators, an emerging class of small molecule therapeutic agents. Allosteric modulation may offer more sophisticated ways to normalize biological signaling compared to classical orthosteric agonist or antagonist drugs. Allosteric, literally translated from its Greek roots, means: other site. Thus, allosteric modulators bind receptors at sites that are distinct from the binding sites of classical small molecule “orthosteric” agonist and antagonist drugs.

The most advanced drug candidate, ADX10059, a negative allosteric modulator (NAM) of metabotropic glutamate receptor 5 (mGluR5), recently demonstrated clinically and statistically significant efficacy in separate Phase IIa clinical trials in gastroesophageal reflux disease (GERD) patients and migraine headache patients. Data from another Phase IIa clinical trial of ADX10059 in acute anxiety are due around the end of 2007.

The Addex discovery capability has previously been validated through a collaboration with Ortho-McNeil, a Johnson & Johnson company. The deal is limited to discovery and development of allosteric modulators of metabotropic glutamate receptor 2 (mGluR2).

In May 2007, Addex completed an initial public offering on the SWX Swiss Exchange, raising CHF137 million ($111 million / €83 million). The IPO was the largest biotech IPO in Europe in three years.

Addex Pharmaceuticals

Disclaimer

The foregoing release contains forward-looking statements that can be identified by terminology such as “not approvable”, “continue”, “believes”, “believe”, “will”, “remained open to exploring”, “would”, “could”, or similar expressions, or by express or implied discussions regarding Addex Pharmaceuticals Ltd, its business, the potential approval of its products by regulatory authorities, or regarding potential future revenues from such products. Such forward-looking statements reflect the current views of Addex Pharmaceuticals Ltd regarding future events, and involve known and unknown risks, uncertainties and other factors that may cause actual results with allosteric modulators of mGluR4, mGluR2 or mGluR5 to be materially different from any future results, performance or achievements expressed or implied by such statements.

There can be no guarantee that allosteric modulators of mGluR4, mGluR2 or mGluR5 will be approved for sale in any market or by any regulatory authority. Nor can there be any guarantee that allosteric modulators of mGluR4, mGluR2 or mGluR5 will achieve any particular levels of revenue (if any) in the future.

In particular, management’s expectations regarding allosteric modulators of mGluR4, mGluR2 or mGluR5 could be affected by, among other things, unexpected actions by our partners, unexpected regulatory actions or delays or government regulation generally; unexpected clinical trial results, including unexpected new clinical data and unexpected additional analysis of existing clinical data; competition in general; government, industry and general public pricing pressures; the company’s ability to obtain or maintain patent or other proprietary intellectual property protection. Should one or more of these risks or uncertainties materialize, or should underlying assumptions prove incorrect, actual results may vary materially from those anticipated, believed, estimated or expected. Addex Pharmaceuticals is providing the information in this press release as of this date and does not undertake any obligation to update any forward-looking statements contained in this press release as a result of new information, future events or otherwise.

Addex Pharmaceuticals

Parkinson’s disease is caused by the progressive death of the neurons responsible for producing dopamine, a neurotransmitter closely linked with movement control. The disease is usually diagnosed when 50 to 80% of these neurons are already dead, and there is currently no medication to stop that process.

The Université Laval research team’s findings could help prevent the disease and, potentially, slow down its progression.

The researchers observed that when mice were fed an omega-3 rich diet, they seemed immune to the effect of MPTP, a toxic compound that causes the same damage to the brain as Parkinson’s. “This compound, which has been used for more than 20 years in Parkinson’s research, works faster than the disease itself and is just as effective in targeting and destroying the dopamine-producing neurons in the brain,” points out Calon.

By contrast, another group of mice that were fed an ordinary diet developed the characteristic symptoms of the disease when injected with MPTP, including a 31% drop in dopamine-producing neurons and a 50% decrease in dopamine levels.

Analyses revealed that omega-3 fatty acids — in particular DHA (docosahexaenoic acid), a specific type of omega-3 — had replaced the omega-6 fatty acids already present in the brains of the mice that had been given omega-3 supplementation.

“This demonstrates both the importance of diet on the brain’s fatty acid composition and the brain’s natural inclination for omega-3 fatty acids,” observes Calon. Since concentrations of other types of omega-3′s had remained similar in both groups of mice, researchers suggest that the protective effect against Parkinson’s comes essentially from DHA.

Another conclusion to be drawn from this finding is that a brain containing a lot of omega-6 fatty acids may be a fertile ground for Parkinson’s disease. These fatty acids, abundant in foods rich in either vegetable oil or animal fat, are already under suspicion for their role in the body’s inflammatory response, cardiac disease, arthritis, and Alzheimer’s. In a balanced diet, the ratio between omega-6 and omega-3 fatty acids should be 4 to 1. However, the average Western diet contains 10 to 20 times more omega-6′s than omega-3′s.

“In North America, the average intake of DHA is between 60 to 80 mg a day, while experts recommend a daily minimum of 250 mg,” explains Calon. “Our results suggest that this DHA deficiency is a risk factor for developing Parkinson’s disease, and that we would benefit from evaluating omega-3′s potential for preventing and treating this disease in humans,” concludes the researcher.

“In recent years we have been able to identify highly specific patterns of abnormal metabolic activity in patients with Parkinson’s disease. These patterns can be quantified with high reliability using PET imaging,” said David Eidelberg, M.D., Director of the Center for Neurosciences at The Feinstein Institute for Medical Research, and senior author of the new publication. “In particular, the brain network associated with abnormal motor function demonstrates increasingly higher levels of activity as Parkinson’s disease progresses. Existing treatments for Parkinson’s symptoms including drug therapies and deep brain stimulation are known to suppress this abnormal brain network.”

“In this publication,” Dr. Eidelberg continued, “we report that the previously published safety and tolerability seen in the Phase 1 open label study of Neurologix’s Parkinson’s disease treatment was also associated with a significant reduction in abnormal network activity in patients receiving the experimental treatment. Moreover, the degree of reduction in this biomarker correlated with the clinical benefit that the treated patients experienced.”

In the Phase 1 study, the investigators injected an adeno-associated virus (AAV) vector carrying an inhibitory gene (glutamic acid decarboxylase or “GAD”) into one side of the subthalmic nucleus (STN) of the brain of 12 patients with advanced Parkinson’s disease. The GAD gene was intended to increase the synthesis of the major inhibitory neurotransmitter in the brain, gamma-aminobutyric acid, or “GABA”, and thus calm the overactive STN. Although all patients had symptoms on both sides of their bodies, the gene transfer procedure was performed on only one side of the brain, enabling the untreated side to serve as a study control. Improvements in both clinical symptoms and abnormal brain network activity were seen predominately on the treated side of the brain at six months following treatment. Both the clinical benefit and the metabolic improvement persisted through the 12 months of the study period. Moreover, the improvements in brain metabolism occurred in areas of the motor network different from those known to be produced by brain lesioning alone. At the same time, the activity of the cognition-related brain network did not change following the gene transfer procedure.

“We are very encouraged by these findings,” said John Mordock, Neurologix President and Chief Executive Officer. “They clearly support the previously reported results from this study, published earlier this year in The Lancet. Moreover, they also suggest a highly useful, measurable biomarker of efficacy for use in subsequent studies of our gene transfer approach to the treatment of Parkinson’s disease and potentially other neurodegenerative conditions. We expect to begin a Phase 2 study of our approach in Parkinson’s disease within the coming weeks, and believe that we are on track to begin a Phase 1 study in epilepsy.”

About Neurologix

Neurologix, Inc. (NRGX.OB) is a clinical-stage biotechnology company dedicated to the discovery, development, and commercialization of life-altering gene transfer therapies for serious disorders of the brain and Central Nervous System (CNS). Neurologix’s therapeutic approach is built upon the groundbreaking research of its scientific founders and advisors, whose accomplishments have formed the foundation of gene therapy for neurological illnesses. Current company programs address such conditions as Parkinson’s disease, epilepsy and Huntington’s chorea, all of which are large markets not adequately served by current therapeutic options.

Cautionary Statement Regarding Forward-looking Statements

This news release includes certain statements of the Company that may constitute “forward-looking statements” within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended, and which are made pursuant to the Private Securities Litigation Reform Act of 1995. These forward-looking statements and other information relating to the Company are based upon the beliefs of management and assumptions made by and information currently available to the Company. Forward-looking statements include statements concerning plans, objectives, goals, strategies, future events, or performance, as well as underlying assumptions and statements that are other than statements of historical fact. When used in this document, the words “expects,” “promises,” “anticipates,” “estimates,” “plans,” “intends,” “projects,” “predicts,” “believes,” “may” or “should,” and similar expressions, are intended to identify forward-looking statements. These statements reflect the current view of the Company’s management with respect to future events. Many factors could cause the actual results, performance or achievements of the Company to be materially different from any future results, performance or achievements that may be expressed or implied by such forward-looking statements, including, but not limited to, the following:

- The Company is still in the development stage and has not generated any revenues. From inception through September 30, 2007, it incurred net losses and negative cash flows from operating activities of approximately $26.2 million and $20.3 million, respectively. Management believes that the Company will continue to incur net losses and cash flow deficiencies from operating activities for the foreseeable future. Because it may take years to develop, test and obtain regulatory approval for a gene-based therapy product before it can be sold, the Company likely will continue to incur significant losses for the foreseeable future. Accordingly, it may never be profitable and, if it does become profitable, it may be unable to sustain profitability.

- The Company will need to conduct future clinical trials for treatment of Parkinson’s disease using the Company’s NLX technology. If the trials prove unsuccessful, future operations and the potential for profitability will be materially adversely affected and the business may not succeed.

- There is no assurance as to when, or if, the Company will be able to successfully receive approval from the FDA on its Investigational New Drug Application to commence a Phase I safety trial for the treatment of epilepsy.

Other factors and assumptions not identified above could also cause the actual results to differ materially from those set forth in the forward-looking statements. Additional information regarding factors that could cause results to differ materially from management’s expectations is found in the section entitled “Risk Factors” in the Company’s 2006 Annual Report on Form 10-KSB. Although the Company believes these assumptions are reasonable, no assurance can be given that they will prove correct. Accordingly, you should not rely upon forward-looking statements as a prediction of actual results. Further, the Company undertakes no obligation to update forward-looking statements after the date they are made or to conform the statements to actual results or changes in the Company’s expectations.

Andrew Feigin, MD, and David Eidelberg, MD, of The Feinstein Institute for Medical Research collaborated with Michael Kaplitt, MD, of Weill Cornell Medical Center in Manhattan and others to deliver genes for glutamic acid decarboxylase (or GAD) into the subthalamic nucleus of the brain in Parkinson’s patients. The study was designed as a phase I safety study, and the genes were delivered to only one side of the brain to reduce risk and to better assess the treatment.

A recently published study included the clinical results of the novel gene therapy trial, but this new report from the same study focuses on the power of modern brain scans to show that the gene therapy altered brain activity in a favorable way. This latest study is published this week in the Proceedings of the National Academy of Sciences.

The patients only received the viral vector-carrying genes to the side of the brain that controls movement on the side of their body most affected by the disease. It was a so-called open-label study — everybody received the gene therapy so the scientists knew that there could be a placebo effect. That is why brain scans were so critical to the experiment. Dr. Eidelberg and his colleagues pioneered the technology and used it to identify brain networks in Parkinson’s disease and a number of other neurological disorders.

In Parkinson’s, they identified two discrete brain networks — one that regulates movement and another that affects cognition. The results from the brain scan study on the gene therapy patients show that only the motor networks were altered by the therapy. “This is good news,” said Dr. Eidelberg, the senior investigator of the study. “You want to be sure that the treatment doesn’t make things worse.” The gene makes an inhibitory chemical called GABA that turns down the activity in a key node of the Parkinson’s motor network. The investigators were not expecting to see changes in cognition, and the scans confirmed that this did not occur.

Position emission tomography (PET) scans were performed before the surgery and repeated six months later and then again one year after the surgery. The motor network on the untreated side of the body got worse, and the treated side got better. The level of improvements in the motor network correlated with increased clinical ratings of patient disability, added Dr. Feigin.

“Having this information from a PET scan allows us to know that what we are seeing is real,” Dr. Eidelberg added. The scans also detected differences in responses between dose groups, with the highest gene therapy dose demonstrating a longer-lasting effect. “This study demonstrates that PET scanning can be a valuable marker in testing novel therapies for Parkinson’s disease,” he said.

The gene therapy technique was developed by Neurologix Inc., a New Jersey-based company. Scientists are now working on a design for a phase 2 blinded study that would include a larger number of patients to test the effectiveness of the treatment.