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Multiple Sclerosis Institute
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NINDS: Blood-Clotting Protein Could be a Target for Therapy against MS

In multiple sclerosis (MS), the immune cells that patrol our blood for pathogens venture out of the bloodstream and attack the brain. Researchers have found that leakage of a blood-clotting protein into the brain, once considered merely a sign of damage in the MS brain, helps stimulate this attack.

In experiments on mice, the researchers were able to block the protein's effect on immune cells – and reduce the clinical signs of MS – without affecting the protein's vital role in blood clotting. Their findings appear in the Journal of Experimental Medicine,* and offer hope for new therapies against MS, the most common disabling neurological disorder of young adults.

Katerina Akassoglou, Ph.D., the study's senior investigator and an assistant professor of pharmacology at the University of California in San Diego, says she hopes the work will lead to improved drugs for MS. Various immunosuppressants are used to modify the course of MS, which can cause recurrent bouts of vision loss, weakness, and even paralysis, but there is currently no cure.

MS occurs when immune cells react against myelin – a protective sheath that insulates neurons in the brain. Why this inflammatory reaction occurs is unknown, but a rupture of the blood-brain barrier appears to be a key event. This structure normally keeps immune cells and microbes from creeping out of the blood and entering brain tissue. Breaks in the barrier – and leakage of the blood-clotting protein fibrinogen – are commonly observed near areas of myelin destruction, but until now, no one realized that fibrinogen might be more than a bystander.

"In brain tissue affected by MS, there's a striking co-localization of fibrinogen with areas of inflammation [a buildup of immune cells] and demyelination," says Dr. Akassoglou, who is supported by the National Institute of Neurological Disorders and Stroke (NINDS). "This led us to the idea that fibrinogen might be an active participant in the disease."

She suspected that fibrinogen – which helps stimulate platelets in the blood to form clots – might also stimulate microglia, the brain's resident immune cells. Prior studies suggest that microglia protect the brain by gobbling up toxins and debris, but that they can also participate in inflammatory reactions. Moreover, they are known to possess a receptor for fibrinogen, called Mac-1.

In an initial experiment, Dr. Akassoglou grew microglia in a laboratory dish and exposed them to fibrinogen. The cells "underwent dramatic changes," she says, swelling up and becoming capable of ingesting other cells.

Next, she probed fibrinogen's role in experimental autoimmune encephalomyelitis (EAE), an MS-like disease that can be induced in mice by sensitizing their immune systems to myelin. In one experiment, she gave mice with the disease ancrod – an anticoagulant, or anti-clotting drug. Mice that received the drug after their first bout of paralysis steadily regained their motor functions, while untreated mice tended to relapse.

Since chronic use of anticoagulants could cause hemorrhaging, Dr. Akassoglou sought a way to specifically inhibit the damaging effects of fibrinogen in the brain without affecting its beneficial effects in blood clotting.

She focused on a small fragment of fibrinogen known to bind exclusively to the Mac-1 receptor. She guessed that a synthetic version of this fragment – or peptide – might serve as a decoy, tying up the receptor and keeping the microglia from responding to the real protein. Indeed, when delivered daily via a nasal spray, the peptide protected mice against EAE induction. It also enhanced motor performance and reduced demyelination in mice that already had EAE. Importantly, the peptide had no effect on blood clotting.

"This is proof of principle that we can block the inflammatory effects of fibrinogen in the brain without impairing its role in blood clotting," says Dr. Akassoglou. "We are very interested in exploring whether this peptide or other fibrin-depleting agents would be safe and effective in MS patients." Antibodies or small molecules that target fibrinogen may prove to be suitable for drug development, she says.


U.S. Pharmacist: Managing Central Pain Syndromes

Central pain is defined as pain associated with lesions of the central nervous system that lead to damage of somatosensory pathways.1 It is considered to be one of the most distressing forms of chronic pain and can be intractable in many patients. Central pain can be nociceptive and/or neuropathic in nature and can be precipitated by trauma, stroke, multiple sclerosis, or compression of cranial nerves. Patient history is the most effective means for diagnosing central pain, and each syndrome is associated with its own array of cardinal symptoms. Central pain syndromes are difficult to manage, and complete pain relief is often unattainable. Reducing pain to a level that is acceptable for the patient should be the primary goal of therapy. This article will focus on pharmacologic therapies that have been evaluated in spinal cord–related pain, brain-related pain, multiple sclerosis–related pain, and trigeminal neuralgia.

Spinal Cord–Related Pain
Trauma is the most common cause of spinal cord–related pain, with an incidence rate ranging from 6.4% to 94% according to published estimates.1 Pain after spinal cord injury can occur immediately or can be delayed for up to five years. When the onset of pain is delayed beyond one year, more than half of such patients may suffer from a pathologic lesion in the spinal cord that expands and damages the center of the cord, a condition known as syringomyelia.2 Although the quality of pain described can vary between patients, there are three common components: spontaneous steady, spontaneous neuralgic, and evoked pain. Spontaneous steady pain may occur as a result of deafferentation of sensory nerves in the central nervous system, resulting in pain that is expected yet unpredictable. Spontaneous neuralgic pain may be derived from neural damage and is most commonly described as a burning sensation. Evoked pain consists of allodynia and/or hyperpathia, conditions where nonnoxious stimuli such as light touch provoke pain. In any case, classifying pain related to spinal cord injury can be challenging due to poor localization and drastic temporal variations. In 2000, an International Association for the Study of Pain (IASP) task force developed a classification system for patients with spinal cord–related pain that identifies the pain type, system involved, and structures or pathology.2

Brain-Related Pain
The majority of cases of brain-related central pain are caused by strokes. Brain-related central pain is rare and occurs in only 1% to 2% of all stroke patients, with 90% arising from vascular etiology.1 Central poststroke pain (CPSP) has been referred to as "thalamic pain," but this term has fallen out of favor in light of evidence showing that pain can arise from numerous sites within the brain. Furthermore, it has been suggested that CPSP can arise from a chemical imbalance between glutamate and gamma-aminobutyric acid (GABA). By correcting this imbalance, pain relief is possible.1,2 Onset of CPSP can occur within one to two months after a cerebrovascular accident, but may be delayed for as long as one to six years after injury. The predominant characteristics are steady and evoked pain, although neuralgic pain is still present. Similar to spinal cord–related pain, there is vast interpatient variability in CPSP. Common symp­ ­ ­ toms include: muscle pain, dysesthesias, hyperpathia, allodynia, intermittent shooting/lancinating pain, circulatory pain, and peristaltic/visceral pain.2

Management of Spinal Cord–Related and Brain-Related Pain
Nonopioid (i.e., NSAIDs) and opioid analgesics are virtually ineffective for the management of spinal cord–related or brain-related central pain. Other therapeutic classes that have been investigated include anticonvulsants, antidepressants, N -methyl-d-aspartate (NMDA) receptor antagonists, and GABA agonists. Based on evidence from small, double-blind, placebo-controlled trials, intravenous lidocaine, ketamine, or propofol may be beneficial for short-term pain control (up to 45 minutes, 30 minutes, and 3 hours, respectively).3-5 Unfortunately, the chronicity of central pain warrants the use of agents that provide long-term relief. Amitriptyline or lamotrigine can be considered as first-line therapy (TABLE 1).6 Amitriptyline use was associated with a reduction in pain and improvement in patient global rating when used in doses of 75 mg po daily over four weeks in a small, double-blind, placebo-controlled trial of 15 patients with CPSP.7 Vestergaard et al8 identified that the titration of lamotrigine up to 200 mg po daily over eight weeks was associated with a reduction in pain scores when compared to placebo in a small group of patients with CPSP. When evaluated in patients with spinal cord–related pain, lamotrigine use resulted in a reduction in brush-evoked allodynia (pain evoked by an innocuous brush) and wind-up-like pain (pain caused by repeated prickling of the skin).9 Second-line therapies include mexiletine, fluvoxamine and gabapentin; the data supporting the use of these agents, however, are based on poor-quality studies and/or anecdotal experience.


Opexa Therapeutics Completes Patient Enrollment in Phase IIb Trial of Tovaxin(TM) for Treatment of Multiple Sclerosis

THE WOODLANDS, Texas, May 17, 2007 (BUSINESS WIRE) --
Opexa Therapeutics, Inc. (NASDAQ:OPXA), a company involved in the development and commercialization of cell therapies, today announced the completion of patient enrollment in a 150-patient Phase IIb safety and efficacy study (TERMS). The trial design is a U.S. multicenter, randomized, double-blind, placebo-controlled study of subcutaneous Tovaxin(TM) in subjects with Clinically Isolated Syndrome (CIS) or Relapsing/Remitting Multiple Sclerosis (RRMS).

Patients participating in the study, which is being conducted under Opexa's U.S. Investigational New Drug (IND) application filed with the U.S. Food and Drug Administration (FDA), will receive 52 weeks of treatment and will undergo safety and efficacy assessments using primary criterion of gadolinium-enhancing lesions and secondary criterion of annualized relapse rate. The Company will collect descriptive analysis data on the first 75 subjects to reach 6 months evaluable later this year. This trial was specifically designed, with the assistance of well-known multiple sclerosis experts, to address three important objectives: to rigorously assess the safety and efficacy of Tovaxin, to maintain a robust clinical effect for the full study, and to provide a scientific and clinical database for advancement to Phase III.

David McWilliams, president and chief executive officer of Opexa Therapeutics, stated, "Full enrollment in this Phase IIb study is an important milestone in the commercialization of Tovaxin. With this milestone achieved, we now look forward to reporting a descriptive analysis in the fourth quarter of 2007 and the full data results in the second half of 2008." McWilliams continued, "I am convinced that the ability to rapidly enroll this study across 35 U.S. centers reflects the high level of interest by multiple sclerosis patients in new safe and effective treatments."

Edward Fox, MD, PhD and lead principal investigator for the Phase IIb study, commented, "If the results of this study can replicate the safety and effectiveness demonstrated in earlier studies, I believe Tovaxin could be an important advance in treating patients with MS. I'm pleased that the positive response from physicians and their MS patients across the country has resulted in the rapid enrollment of this study."

About T-cell Vaccination

For a T-cell vaccine to be effective, it should be able to induce T-cell cytotoxic and/or regulatory immune responses against the pathogenic T-cells. Studies of T-cell vaccine have indicated that T-cell vaccination with peripheral blood-derived autologous myelin-peptide selected T-cells in multiple sclerosis patients resulted in the in vivo induction of CD8+ cytotoxic T-cells and CD4+CD25+FoxP3 Tregs specific for T-cell vaccine. The induction of anti-idiotypic cytotoxic CD8+ effector T-cells and anti-ergotypic CD4+CD25+FoxP3 positive Tregs is believed to provide a therapeutically effective dual mechanism of protection to patients treated with Tovaxin(TM). The observed regulatory immune responses have been shown to collectively correlate with clinical improvement in treated patients.


The Tovaxin Phase IIb clinical study will include 150 patients in a multicenter, randomized, double blind, placebo-controlled trial designed primarily to evaluate the efficacy, safety and tolerability of the Tovaxin T Cell vaccination with clinically isolated syndrome (CIS) and relapsing-remitting MS (RR-MS) patients. A total of 100 patients will receive Tovaxin, while 50 will receive placebo. The study is designed as a two-arm, 52-week, parallel-group study, whereby patients will be given five subcutaneous injections at 0, 4, 8, 12 and 24 weeks. The analyses will be performed at the end of the 52-week study to assess the safety and efficacy of Tovaxin. The primary efficacy variable is the cumulative number of gadolinium-enhancing lesions on T1-weighted MRI scans summed over the Week 28, 36, 44, and 52 MRIs. The secondary efficacy variables are the cumulative number of new gadolinium-enhancing lesions at Weeks 28-52, the change in T2-weighted lesion volume, and the annualized relapse rate.

All patients who complete the trial will be eligible to participate in an optional one-year extension study, in which they will receive Tovaxin under an open-label protocol. The open-label study is being planned under a different protocol that will be submitted to the FDA.

About Opexa Therapeutics

Opexa Therapeutics develops and commercializes cell therapies to treat autoimmune diseases such as MS, rheumatoid arthritis, and diabetes. The Company is focused on autologous cellular therapy applications of its proprietary T-cell and stem cell therapies. The Company's lead product, Tovaxin(TM), a T-cell therapy for multiple sclerosis is in Phase IIb trials. The Company holds the exclusive worldwide license for adult multipotent stem cells derived from mononuclear cells of peripheral blood. The technology allows large quantities of monocyte derived stem cells to be produced efficiently for use in autologous therapy, thus circumventing the threat of rejection. The Company is in preclinical development for diabetes mellitus. For more information, visit the Opexa Therapeutics website at

Safe Harbor Statement

This press release contains "forward-looking statements," including statements about Opexa Therapeutics' growth and future operating results, discovery and development of products, strategic alliances and intellectual property, as well as other matters that are not historical facts or information. These forward-looking statements are based on management's current assumptions and expectations and involve risks, uncertainties and other important factors, specifically including those relating to Opexa Therapeutics' ability to obtain additional funding, develop its stem cell technologies, achieve its operational objectives, and obtain patent protection for its discoveries, that may cause Opexa Therapeutics' actual results to be materially different from any future results expressed or implied by such forward-looking statements. Opexa Therapeutics undertakes no obligation to update or revise any such forward-looking statements, whether as a result of new information, future events or otherwise.

Testosterone May Help Men with Multiple Sclerosis

05/15/07 -- A small pilot study suggests that testosterone treatment is safe, well tolerated and may reduce symptoms, slow brain degeneration and increase muscle mass in men with relapsing-remitting multiple sclerosis, the most common form of the disease, according to a report in the May issue of Archives of Neurology, one of the JAMA/Archives journals.

Multiple sclerosis is a progressive disease involving the immune and central nervous systems. MS and many other autoimmune diseases (in which the body attacks its own systems or tissues) are less common in men than in women, according to background information in the article. This is especially true during reproductive years. Sex hormones, including testosterone and estrogen, may be responsible for the difference. Testosterone has been shown to protect against an MS-like condition and other autoimmune diseases in animals.

Nancy L. Sicotte, M.D., of the David Geffen School of Medicine at UCLA, Los Angeles, and colleagues conducted a study of testosterone treatment in 10 men with relapsing-remitting MS, characterized by periods of neurologic symptoms (such as numbness or difficulty walking) followed by periods of remission. The men, who had an average age of 46, were enrolled in the study and then entered a six-month pre-treatment phase, during which symptoms were monitored but no therapies were administered. Then, each man applied 10 grams of a gel containing 100 milligrams of testosterone to his upper arms once daily for 12 months.

"One year of treatment with testosterone gel was associated with improvement in cognitive performance and a slowing of brain atrophy [deterioration]," the authors write. During the first nine months of the study--the period of time before the men began taking testosterone, plus the first three months of treatment, before it had time to take effect--brain volume decreased an average of -0.81 percent per year. In the second nine months, this decline slowed by 67 percent to an annual rate of -0.25 percent. "Because the protective effect of testosterone treatment on brain atrophy was observed in the absence of an appreciable anti-inflammatory effect, this protection may not be limited to MS, but may be applicable to those with non-inflammatory neurodegenerative diseases," including amyotrophic lateral sclerosis or Lou Gehrig's disease, the authors write.

In addition, lean body mass (muscle mass) increased an average of 1.7 kilograms (about 3.74 pounds) during the treatment phase. Participants did not report any adverse effects, there were no abnormalities in blood tests taken during the trial and the men's prostate examination results remained stable.

"Overall, in this first trial of testosterone treatment in men with relapsing-remitting MS, the treatment was shown to be safe and well tolerated," the authors conclude. "In addition, exploratory findings reported herein suggest a possible neuroprotective effect of testosterone treatment in men, which warrants further investigation."


Research key to mysteries of MS

DID you know that Edinburgh and the Lothians can make a reasonable case for having the highest rate of multiple sclerosis in the world? More than 1500 people in the area have the condition, which normally strikes between the ages of 20 and 40.

One of the unanswered riddles of MS is why it should be more common in Scotland than anywhere else (nearly twice as common as in the south of England, for example). Mysteriously, MS is generally more common the further you go north or south from the equator. It is also three times more likely to affect women than men. Appropriately enough, Edinburgh is now also home to some of the world's leading research into the disease.

In someone suffering from Multiple Sclerosis, the insulation around nerve cells in the brain and spinal cord gets damaged. It seems that the body's immune system, which normally attacks harmful intruders like viruses, gets confused and starts attacking the nerve cells. Depending on which cells get damaged, a great variety of symptoms can result, including sight problems, tremor, bladder and bowel difficulties, pain and difficulties with balance and walking.

But it is often fatigue, an invisible symptom, which people with MS will highlight. This is not just a bit of tiredness but an overwhelming and incapacitating inability to carry out normal tasks. And because it is invisible, fatigue is a symptom which is not well recognised or understood by the general public, something which is also true of the thinking and memory difficulties which can sometimes occur.

MS varies between people and is very unpredictable. Often MS starts with an attack of symptoms, which then subside for a period before further attacks.

The frequency and severity of the attacks vary. Some people have fewer regular attacks but experience a gradual deterioration in symptoms over many years. Some people have MS for decades and you would never know. So one of the most difficult things which people with MS have to deal with from the point at which they are diagnosed is the uncertainty of what will happen. Plus, of course, all the normal stuff that everyone deals with - education, jobs, relationships, children, money - which can become an extra challenge when you are already coping with MS.

As yet, scientists have been unable to identify what causes MS. It is known to be some combination of genetic and environmental factors. While MS is not an inherited condition it can be more common in some families. For genetically identical twins, if one gets MS the other twin has around a 30 per cent chance of also getting MS.

So far as the environmental triggers of MS are concerned, a huge number of different theories have been proposed but all remain unproven. Suggested risk factors have included a variety of viruses, diet, smoking, dental fillings, head injury, exposure to dogs and toxins. Recently the idea that vitamin D deficiency may play a part has been suggested. There seems to be mounting evidence that the long, dreich Scottish winter leaves large parts of the general population deficient in this vitamin. Certainly, MS is less common in sunny Mediterranean climes. But then, just as you think a clear pattern may be emerging, you find that MS turns out to be quite common in Sardinia. Nothing in MS is simple or straightforward.

Encouragingly, great efforts are being made by researchers at Edinburgh University to unravel some of the mysteries of MS. Professor Peter Brophy is doing world-leading research into finding the molecules which stick the insulation on to nerve cells. This could help understanding of what goes wrong in MS and eventually provide targets for new drug treatments. Dr Steve Anderton is researching the immune system and trying to find ways to stop it attacking the nerve cells.

Most recently, the MS Society has teamed up with the university to create a new Centre for Translational Research. The centre aims to develop ways of repairing the damage done in MS. It is hoped that this will be done either by switching on the brain's own ability to repair itself or by transplanting cells into the body.

But while these are exciting possibilities, the timescale for the arrival of these treatments is unfortunately counted in years, not months. The MS Society is the major funder of research in Scotland. Currently backing projects costing over £4m, the society relies on public support to continue its work.

While much remains to be learned about the causes of MS, there is a huge amount known about the support people affected by MS need. Happily, recent years have seen significant improvements in some of the services available to people locally. A specialist clinic has been set up at the Western General hospital, with a neurologist, specialist nurses and a specialist physiotherapist. Rehabilitation services at the Astley Ainslie hospital are well developed and can help people maintain independence. The MS Society has recently completed a successful project to provide training in MS to health and social care staff across the Lothians. It makes a big difference to people affected by multiple sclerosis if the staff they come into contact with have a basic knowledge and awareness.

But progress isn't uniform. For example, the local authority budgets which allow the carer of someone with MS to get a break have been reduced. You could be providing support 24/7 to your partner year-round yet still get no support for the vital break which will help you keep going. So although North Berwick is the home of the MS Society's respite care centre you may not get local authority help to access this excellent service.

It is part of the work of the MS Society to keep up the pressure on issues like this, as well as funding research and services like specialist nurses and grants. In the Lothians, such resources have never been better, but there remains a lot of work to do on all fronts.

• Mark Hazelwood is director of MS Society Scotland. To support the work of the MS Society contact f For more information, log on to or call the MS Society Helpline 0808 800 8000

Analysis: Early MS therapy delays decline

By ED SUSMANBOSTON, May 2 (UPI) -- The risk that a multiple sclerosis patient will decline in function can be dramatically reduced if that patient is treated at the first sign of an attack, U.S. researchers said Tuesday.

"For the first time we are showing that treating people early (means) not only preventing attacks, but significantly delaying disability," Mark Freedman, director of the Multiple Sclerosis Unit at the University of
Ottawa, told United Press International.

In a presentation Tuesday at the 59th annual meeting of the American Academy of Neurology in
Boston, Freedman said that treating patients early in the disease course with interferon beta-1b -- sold as Betaseron and a standard-of-care drug for MS for two decades -- resulted in:
-- a 40-percent reduction in the risk of progression as measured by standard on disability tests. "About 24 percent of placebo patients showed disease progression on the Expanded Disability Scale Score compared with 16 percent of patients on Betaseron," Freedman told UPI.

-- a 41-percent reduction in the risk that patients will have a second MS attack within three years. "About 51.7 percent of patients who were started on placebo suffered a multiple sclerosis confirming attack within three years of the study compared with 36 percent of people on Betaseron," he said.

Traditionally, doctors have waited until a second "confirmatory" MS exacerbation occurs before starting treatment -- but the BENEFIT (Betaseron in Newly Emerging Multiple Sclerosis for Initial Treatment) trial challenges that theory.

"I was one of those skeptics who told patients who had one multiple sclerosis attack that we could afford to wait," Freedman admitted, but now he said that it appears early treatment does benefit patients.

His study involved 468 patients, originally assigning 261 patients to Betaseron and 157 to placebo. After three years 249 patients remained on the interferon treatment and 143 patients were still on placebo.

Freedman said that patients who had second attacks and then began interferon therapy did not catch up to the patients who began with active treatment after the first signs of multiple sclerosis. "The differences between these groups continue to widen," he said.

"Some patients have already developed significant neurological damage when they first present with signs of multiple sclerosis, which can lead to accumulated disability later in life," Freedman said.

"This is a truly novel finding that has not yet been demonstrated for any other immunomodulatory multiple sclerosis treatment, and underscores the urgent need to treat patients early, rather than waiting for further signs of disease to develop," he added. "Physicians and patients should consider these unprecedented findings when making treatment decisions."

Freedman said patients who have a first attack have an 80-percent chance of having a second attack within two years. "Immediate treatment can prevent or delay the chance of progression," he said.

"We now have very persuasive data that treating early is a better course of action," said Gary Birnbaum, director of the Multiple Sclerosis Treatment and Research Center at the
Minneapolis Clinic of Neurology in Golden Valley and a board-certified neurologist.

"The new study shows us that the placebo patients never quite catch up to the patients who are treated after the first attack. I think the general consensus now is that patients should be treated as soon as they meet the most recent criteria for multiple sclerosis."

He said that neurologists using a combination of clinical examination and imaging data can make an accurate diagnosis after that initial attack.


'Surviving General Motors': Former Employee Describes Harassment at GM, Corruption of Legal System in New Book

WEST BLOOMFIELD, Mich., May 1 /PRNewswire/ -- Americans expect to receive basic rights, equality and freedoms granted by the Bill of Rights and protected by the U.S. legal system. In her new book, "Surviving General Motors with Multiple Sclerosis: Questions of Conscience, Morality and Leadership" (now available through AuthorHouse), Zohar McMillan details the legal battle that ensued when she believed these basic rights were violated during her employment at a General Motors Corp. plant.

For years, McMillan was a dedicated GM employee; she loved her job as a journeyman electrician. Her experience changed drastically, however, when she was reassigned to the Pontiac Assembly Center. McMillan recalls disturbing details of what she claims was unrelenting harassment by co-workers and superiors alike. Included in her list of allegations are discrimination due to her Multiple Sclerosis, denial of proper safety rights and medical attention, threats of physical violence by a general foreman, extremely disturbing racial slurs and gender-based insults.

Taking legal action, McMillan brought the case before a circuit court in order to bring the trial before a jury, but the judge ruled in favor of GM. "After receiving the judge's written opinion, I went into shock," McMillan says. She decided to appeal. She supplied her attorney with incidences from journals she kept and a right to sue letter issued by the Equal Employment Opportunity Commission.

McMillan hopes the experiences chronicled in "Surviving General Motors with Multiple Sclerosis" will shed light on the injustices that still occur in the workplace. "We have a constitution which all Americans are to abide by, including corporations ... ," she says. "We need to reclaim our courts."

Michigan, the heart of the automobile industry, has been home to McMillan her entire life. A true survivor, she was diagnosed with Multiple Sclerosis 12 years ago. "Surviving General Motors with Multiple Sclerosis" is her first book. Visit for more information.

Virtual reality device helps multiple sclerosis patients walk

Technion-Israel Institute of Technology scientists have created a virtual reality device that combines auditory and visual feedback to improve walking speed and stride length in patients suffering from Multiple Sclerosis (MS) and Parkinson's disease.

According to lead researcher Professor Yoram Baram of the Faculty of Computer Science, the device combines a wearable, cell phone-sized audio component - which measures body movement, processes it and sends feedback to the user through earphones - with a visual feedback apparatus he developed for Parkinson's patients 10 years ago.

The visual component presents users with a virtual, tiled-floor image displayed on one eye via a tiny piece that clips onto glasses worn by the user. This allows the user to distinguish between the virtual floor and real obstacles, making it possible to navigate even rough terrain or stairs.

Baram and Prof. Ariel Miller of the Faculty of Medicine and the Multiple Sclerosis and Brain Research Center at the Carmel Medical Center in Haifa examined the effects of the patented device on the gait quality of MS patients.

The researchers found that auditory feedback significantly improved the gait of both MS and Parkinson's patients (though the improvement was less pronounced in Parkinson's patients).

With regard to walking speed, patients showed an average improvement of 12.84% while wearing the device. There were also positive residual short-term therapeutic effects (18.75% improvement) after use. Average improvement in stride was 8.30% while wearing the device and 9.93% residually.

"Healthy people have other tools, such as sensory feedback from muscles nerves, which report on muscle control, telling them whether or not they are using their muscles correctly," says Baram. "This feedback is damaged in Parkinson and MS patients and the elderly, but auditory feedback can be used to help them walk at a fixed pace."

Results from a small study (14 randomly selected patients with gait disturbances predominantly due to MS) on the device are published in the February 2007 issue of the Journal of the Neurological Sciences.

The integrated device - the first to respond to the patient's motions rather than just providing fixed visual or auditory cues - is already in use at a number of medical centers in Israel and the United States, including the University of Cincinnati and the State University of New York.

The Technion-Israel Institute of Technology is Israel's leading science and technology university. Home to the country's winners of the Nobel Prize in science, it commands a worldwide reputation for its pioneering work in nanotechnology, computer science, biotechnology, water-resource management, materials engineering, aerospace and medicine.

The majority of the founders and managers of Israel's high-tech companies are alumni. Based in New York City, the American Technion Society is the leading American organization supporting higher education in Israel, with 17 offices around the country.


Rituxan, a drug currently used to treat a certain type of cancer and rheumatoid arthritis showed promise in treating patients with the most common form of multiple sclerosis, according to two small studies presented Tuesday involving the drug.

Rituxan, co-marketed by Genentech Inc. and Biogen Idec Inc. was originally approved to treat non-Hodgkin's lymphoma, a cancer of the lymphatic system. It kills B cells or a type of white blood cell.

The studies suggest that targeting such B cells might also be a new way to treat MS, a progressive disease that involves damage to nerves controlling muscles and vision. More specifically, the body attacks myelin, a fatty substance that surrounds the nerve fibers of the brain, spinal cord and optic nerves. Scar tissue, or brain lesions are left behind from the attacks, which can be detected with an MRI scan.

The studies, presented Tuesday at the American Academy of Neurology's annual meeting on Boston, looked at using Rituxan in patients with the relapsing-remitting form of MS, where symptoms flare up and then subside. Overall, the studies showed Rituxan reduced the number of brain lesions and cut the number of relapses.

One of the studies involved 104 patients, 69 of whom received a single course of Rituxan and 35 were given a placebo, or fake treatment. The patients are being followed for 48 weeks, but data from the 24 week mark was released. Rituxan is an infusion and was administered in two courses, two weeks apart.

The number of lesions per patient were reduced by 91% among the Rituxan patients compared to those in the placebo group. About 14.5% of patients receiving Rituxan relapsed compared to 34.3% in the placebo group.

The study's lead researcher Dr. Stephen Hauser, the chair of the neurology department at the University of California, San Francisco, said the data suggests a new pathway to treat MS by targeting B-cells. Other treatments like Tysabri target infection-fighting T-cells in the body to keep them from attacking myelin.

Hauser told Dow Jones Newswires the study results were very encouraging but that larger studies are needed to verify whether Rituxan would be a viable MS treatment. Genentech and Biogen are also studying it a treatment for another form of MS but the results are not yet available. Hauser also said his study wasn't long enough or large enough to address long-term safety questions.

His study showed that more patients receiving Rituxan, or 78.3%, suffered an infusion reaction compared to 40% in the placebo group. Such reactions included flu-like illness, fever and low blood pressure.

In December, Genentech and Biogen Idec warned that two patients being treated for lupus with Rituxan contracted a viral brain infection known as progressive multifocal leukoencephalopathy, or PML. Rituxan is not approved as a lupus treatment but the companies are also studying the drug for that use.

Hauser said the results from his study involving Rituxan as an MS treatment look as encouraging as the early clinical data for did for Tysabri, another MS treatment.

Tysabri, also by Biogen Idec and Elan Corp. (ELN), was taken off the market in 2005 after three patients developed PML but was allowed to return last year with strict warnings and a restricted distribution plan.

A second study involved 26 people who received Rituxan at the study start and then six months later. It also showed brain lesions were reduced by more than 90% and that the expected relapse rate was cut in the patients who were followed for at least a year. The study did not involve a placebo group and was partly designed to look at whether it was safe to use Rituxan in MS patients. CLICK FOR MORE

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Biogen, Elan Get No New Reports Of Brain Infection From Tysabri


WASHINGTON -- There have been no additional reports of a serious brain infection known as progressive multifocal leukoencephalopathy, or PML, among patients taking the multiple-sclerosis drug Tysabri, the drug's makers said Thursday.

Biogen Idec Inc. and Elan Corp., also said there were no reports of other "serious opportunistic infections," as of April 23. The companies released the first safety update involving Tysabri since the drug was allowed back in the U.S. market last June. The data was released at the American Academy of Neurology's annual meeting on Boston.

The drug was pulled off the U.S. market in February 2005 after two patients developed PML and one died. A third patient was later discovered to have PML and also died.

Tysabri is currently under a restricted distribution system and a program that allows the companies to track potential safety problems with the drug.

The companies said about 12,500 patients world-wide have been prescribed Tysabri, including about 6,600 patients in the U.S. currently who are on therapy.

The companies said about 10,000 U.S. patients and 1,500 physicians have enrolled in the restricted distribution program known as Touch. Tysabri is administered as an infusion in a clinic. The FDA recommends the drug be used only after other treatments fail for the relapsing-remitting form of MS. MS is a progressive disease that involves damage to nerves controlling muscles and vision, and affects about 400,000 Americans.

Before Tysabri can be started, patients must undergo a magnetic resonance imaging or MRI scan to differentiate potential future multiple sclerosis symptoms from PML. Patients would then be evaluated at three months, six months and then every six months after that. The status of those evaluations must be reported by doctors to Biogen Idec.

Biogen and Elan also issued an update on an extension study of an original two-year study that involved 942 patients. That study, known as Affirm, showed Tysabri cut the annual risk of relapse by 67% compared with patients on placebo, or a fake drug. The extension study includes 531 patients, 250 who have received almost three years of therapy.

The companies said, the annualized relapse rate for patients treated with Tysabri over the three-year period was 0.23, which translates into an average relapse rate of one relapse every 4.3 years. Over the three-year treatment period, the relapse rate averaged 0.27 during the first year; 0.20 during the second year; and 0.15 during the third year.

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Low-Dose Aspirin Protection Against Cognitive Decline? Think Again

BOSTON, April 27 -- Low-dose aspirin doesn't protect women against overall cognitive decline, a finding that adds to doubts about whether anti-inflammatory drugs offer any neuroprotective benefit.

Among more than 6,000 healthy women who took low-dose aspirin or placebo for a decade, there were no significant between-group differences in overall cognitive function, rate of cognitive decline, or risk for serious decline, reported Jae Hee Kang, Sc.D., of Brigham and Women's Hospital here, and colleagues.

"In this study, we observed no apparent benefit of low-dose aspirin in slowing cognitive decline over four years," the authors wrote online in BMJ. "Other methods for preserving cognitive function in older people need to be investigated."

Women who took aspirin had a 20% lower risk for decline in category fluency, the authors noted, but the effect seen with this secondary endpoint was not enough to tip the scales in aspirin's favor.

Earlier this week, two other NSAIDs were shown to offer no protective benefit against Alzheimer's, investigators reported online in Neurology. Neither naproxen (Aleve) nor celecoxib (Celebrex) reduced the risk of developing Alzheimer's, at least in the short term, found researchers in the ADAPT (Alzheimer's Disease Anti-inflammatory Prevention Trial) study.
According to results of the randomized ADAPT study funded by the National Institute on Aging, there was even a suggestion that both naproxen and celecoxib were associated with a slightly increased risk of dementia.

Interest in the use of NSAIDs for Alzheimer's prevention was sparked by a study, published in Neurology in 1993, indicating that indomethacin in doses of 100 to 150 mg/day appeared to protect mild-to-moderately impaired Alzheimer's patients from the degree of cognitive decline exhibited by well-matched controls.

But results from randomized trials conducted since have been inconclusive or have shown no neuroprotective benefit for the NSAIDs rofecoxib, naproxen, nimesulide, and diclofenac, the ADAPT investigators noted.

In the current study, Dr. Kang and colleagues looked at data from the Women's Health Study, a randomized, double-blind, placebo controlled two-by-two factorial trial of aspirin given in doses of 100 mg on alternate days, and supplementation with vitamin E 600 IU on alternate days. The goal of the trial was to determine whether the combination could protect women against cardiovascular disease and cancer.

The cohort included 6,377 women, mean age 72, from both arms of the study. The women had three cognitive assessments conducted by telephone interview at two-year intervals. They were tested for general cognition, verbal memory, and category fluency.

The primary study outcome was a global cognition score calculated by averaging performance across all tests. The investigators also looked at verbal memory scores, calculated by averaging the performance of volunteers on four measures.

They found that at the first assessment, an average of 5.6 years after randomization, the cognitive performance among women treated with aspirin was similar to that of placebo-treated controls. The mean difference in global score was -0.01 (95% confidence interval, -0.04 to 0.02).

There was also no significant difference between the groups in the mean decline in global score from the first cognitive assessment to the last, with a mean difference of 0.01 (95% CI, -0.02 to 0.04).

The risk that women would be in the highest (worst) 10th percentile of cognitive decline was likewise similar between the aspirin and placebo groups (relative risk 0.92, 95% CI, 0.77 to 1.10), and there were no significant differences in verbal memory scores.

However, women who took aspirin had a slightly lower risk of decline in category fluency, measured by asking the participants to name as many animals as they could in one minute. The relative risk for decline in this measure for aspirin takers versus controls was 0.80 (95% CI, 0.67 to 0.97).

"Because the category fluency test partially assesses executive function -- a cognitive system that is influenced by vascular disease -- it is biologically plausible that low dose aspirin may specifically help preserve executive function," the authors wrote. "However, because category fluency was the only test in our battery that measured executive function, and because this was not a primary outcome of our trial, this result should be interpreted with caution and confirmed by future studies."

Dr. Kang and colleagues noted that their study was limited by the age of the cohort, which was relatively young compared with the total study cohort of women 65 and older, and may have contributed to their failure to see a major cognitive decline over the follow-up period. They also noted that they were unable to measure cognitive decline from randomization, but pointed out that risk factors for cognitive decline were evenly distributed at baseline.


Johns Hopkins Medicine
Media Relations and Public Affairs

Johns Hopkins researchers have identified a backup supply of stem cells that can repair the most severe damage to the nerves responsible for our sense of smell. These reservists normally lie around and do nothing, but when neighboring cells die, the scientists say, the stem cells jump into action. A report on the discovery will appear online next week in Nature Neuroscience.
"These stem cells act like the Army Reserves of our nose," explains lead author Randall Reed, Ph.D., a professor of neuroscience at Johns Hopkins, "supporting a class of active-duty stem cells that help repair normal wear and tear. They don't come in until things are really bad."

The only nerve cells in the body to run directly from the brain to the outside world, olfactory cells are under constant assault from harsh chemicals that one might happen to catch a whiff of by accident, risking damage or death.

To figure out how the olfactory system repairs severely damaged nerve cells, Reed's team exposed mouse olfactory nerves to a cloud of toxic methyl-bromide gas. Methyl bromide kills not only olfactory nerve cells but also neighboring, non-nerve cells in the nasal passage. Three weeks after chemical exposure, the researchers examined nasal cells to see which, if any, had grown back.

They discovered that the newly grown cells, both nerve and non-nerve, grew from HBCs, or horizontal basal cells, a population of cells not previously known for repair abilities. "We were stunned because HBCs normally don't grow much or do anything," says Reed. "And the most surprising thing is that HBCs can grow into both nerves and non-nerve cells; they do so by generating the other active type of nasal stem cell."

The team then went back and looked at nerve repair under less damaging circumstances where only the olfactory nerve cells are killed. In this situation, the HBCs did nothing to repair the damaged cells; rather, they allowed the previously known stem cells to do all the repair work.

"The ability to smell is crucial for eating, mating and survival, and it's important that the olfactory system be fully operational all the time," explains Reed. "The HBCs act as a fail-safe to ensure continued function of the sense of smell."

The discovery of these two distinct types of stem cells in one neural tissue is a first, says Reed, who is interested to see if other types of nerves in the body have similar repair mechanisms in play.

The research was funded by the Howard Hughes Medical Institute and the National Institutes of Health.

Authors on the paper are Cheuk Leung, Pierre Coulombe and Randall Reed, all of Johns Hopkins.

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