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Sold by thrift. Be the first to write a review About this product. About this product Product Information "We now know the answers to helping long time welfare recipients become self-sufficient, and how to pry loose the dead hand of human service bureaucracies. I really like my kids to know I work But the medical establishment has failed stroke patients not just because the research is hard, but because of misaligned incentives, the financial pressures of an industrial drug-development model, and sloppy science.

Others die from complications like pneumonia, which can affect up to one-third of all stroke patients. Stroke weakens the immune system , making it harder for the body to fight lung infections that can occur when stroke victims, who can no longer swallow properly, wind up with food, water, or saliva in their lungs.

For most of history, health workers had no way to help stroke victims. Once a stroke was identified, the patient was made comfortable and family members were given the bad news. Stroke was viewed as a dead end—for patients, for researchers, and for neurologists looking for solutions—and stroke nihilism still permeates the medical establishment.

The bulk of progress in reducing stroke deaths has come from prevention, particularly the introduction of medicines to lower high blood pressure, a leading cause of stroke. The first—and to date only—medical breakthrough for stroke treatment came when a drug called tissue plasminogen activator tPA, sold globally under the brand names Activase and Actilyse was approved by the US Food and Drug Administration FDA in The longer the penumbra is deprived of blood, the less brain there is to save.

With tPA, emergency-room doctors at last had a way to treat patients. But, as with most things in the world of stroke, there were complications. In this case, the issue was that there are two kinds of stroke.

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For that reason, the drug is also not given to patients on blood thinners or who have other complications. There are less than 4. For patients over 80 or those who had a previous stroke, the window is only three hours. Further, tPA is expensive. It also needs to be refrigerated, a challenge for clinics in some parts of the world.

As a result, the use of tPA is limited to affluent nations with sophisticated healthcare systems, and even then it is only rarely administered.

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Since its introduction, tPA has also been plagued by doubts about its safety , stemming from long-standing criticisms of its initial clinical trials. In poorer parts of the world, the number is closer to zero. According to one landmark study, 1, potential neuroprotective drugs were tested between and , in 8, separate experiments. Those failures cost billions of dollars and wasted the productive years of thousands of scientists.

The pharma industry saw more lucrative opportunities elsewhere, and moved on. But not all scientists accepted that conclusion.

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On the fringes of industrial medicine, one neurosurgeon has spent the last two decades doggedly developing a neuroprotective agent. The best hope for stroke patients may come not from the giant research labs of industrial pharma, or the biotech hotbeds of Boston or San Francisco, but from the relative backwater of Toronto, Ontario. Michael Tymianski, now 55, has been working on his drug, called NA-1, since the late s, when researchers were still infused with optimism about developing a stroke treatment. A tall, balding man with a furious work ethic, Tymianski poured himself into developing NA-1 while holding down his day job as a neurosurgeon at a Toronto hospital.

His plan was always to develop the drug to the point where it could be tested in humans, then sell it to a pharma company.

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But no buyers materialized, and eventually Tymianski stopped looking. Instead, in , Tymianski founded his tiny biotech startup, fueled by confidence in the drug based on his critical insight into brain chemistry. Following a stroke, neurons become flooded with calcium, which generates free radicals—unstable molecules with an unpaired electron, like nitric oxide, or NO—which causes havoc in neurons. But Tymianski and his team identified a drug that prevents a protein called PSD from binding within neurons, enabling them to resist that lethal accumulation of NO.

Stroke nihilism

He never set out to become a pharmaceutical executive, but with the pharma industry out of the stroke business, Tymianski was forced to go it alone, bootstrapping funding from friends and neighbors. Put this in a desk drawer and forget about it? I saw this as a natural extension of my obligation as a physician. As German stroke researcher Ulrich Dirnagl notes, neuroprotection has never been proven to work in humans. An advocate of more rigorous statistical analysis of stroke research, Dirnagl informally handicaps the odds of various trials for stroke treatments.

Which is the highest rating I have for any running neuroprotection trial. Tymianski understands the doubts. But NoNO has learned from the failures of the pharma industry, and has constructed its clinical trials to improve the odds of winning regulatory approval and launching NA-1 into the market.

The history of neuroprotection research begins, strangely enough, with Chinese food. The flavor additive monosodium glutamate, commonly known as MSG, was first identified in Japan in by chemist Kikunae Ikeda, who was intrigued by the origins of the umami taste in seaweed. Used for decades without incident, MSG began drawing the attention of the medical community in , when the New England Journal of Medicine published a letter to the editor describing symptoms of numbness and palpitations that the writer, Robert Ho Man Kwok, attributed to eating at Chinese restaurants.

Kwok, himself a recent Chinese immigrant, identified MSG as a possible culprit. Louis, published a paper in Science demonstrating that in mice dosed with MSG, neurons died, leading to brain lesions. The mice in his experiment were injected with, not fed, MSG, and in much higher amounts relative to body size than humans ever ingested. Glutamate is an amino acid found widely in the brain and central nervous system. It lives in the axons—the tendrils at the end of neurons—and plays a critical role in sending messages between those neurons. Once its host neuron sends out the right signal, the glutamate is released, and crosses the synapse, the divide between two neurons.

On the other side of the synapse, the glutamate binds to the receptor of another neuron.