Using Human Neurons to Prevent Brain Injury - Dr. Valina Dawson
Published on Jun 25, 2015#TomorrowsDiscoveries: Millions of Americans suffer from brain injury because of stroke or diseases. Using lab-grown human neurons, Dr. Valina Dawson is working to identify what causes brain cell death. Her research may lead to new treatments to prevent brain injury. Learn more about Dr. Dawson's work: http://ow.ly/PrJIs.
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The Institute for Cell Engineering (ICE) at Johns Hopkins
Published on Dec 13, 2013Neuroscientist Valina Dawson introduces the Institute for Cell Engineering (ICE), where researchers are working to solve problems such as transplant rejection, Parkinson's disease, and coronary artery disease using regenerative medicine. For more information visit http://www.hopkinsmedicine.org/ice.
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#TomorrowsDiscoveries: Keeping Memories Safe - Dr. Ted Dawson
Published on Jun 25, 2015#TomorrowsDiscoveries: Neurons store our memories and control all aspects of our bodily functions; they are what make us human. Dr. Ted Dawson’s research focuses on the culprits that kill neurons. His hope is to find ways to prevent the loss of neurons in Parkinson’s disease, stroke and other brain disorders. Learn more about Dr. Dawson's work: http://ow.ly/PrKKk.
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#TomorrowsDiscoveries: Brain Cells Damaged by Stroke - Dr. Shaida Andrabi
Published on Jun 25, 2015#TomorrowsDiscoveries: After a stroke, brain cells lose their capacity to generate energy. Dr. Shaida Andrabi and his team are working to find out why this happens and how to prevent it. Learn more about Dr. Andrabi’s work: http://ow.ly/Ps1HQ.
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Valina Dawson | Studying Cell Survival and Death in Human Neurons
Uploaded on Aug 31, 2010by Valina Dawson
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A Multi-Chamber Device for Studying Neural Degeneration
Published on Nov 19, 2013A multi-chambered device to study neurodegeneration can reduce rodent use in drug development:
Neurodegeneration is a component of many neurological disorders including multiple sclerosis, stroke and Alzheimer's and Parkinson's diseases. Understanding how to protect neurons from injury and death is a key area of research for new therapies. It is estimated worldwide that 130,000 rats and mice are used to study the cellular and molecular changes that occur during neurodegeneration.
NC3Rs-funded researchers, Professor Hugh Perry and Dr Tracey Newman, University of Southampton, have developed a microfluidic device that creates a suitable environment to study what happens during neuronal injury. This better understanding can inform how drugs are tested at the later stages of development, reducing the number of rodents that would be required.
For more information visit www.nc3rs.org.uk.
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Strokes and Excitotoxicity Part 1
Published on Oct 29, 2014SSTattler: Four parts "Strokes and Excitotoxicity" and the "mechanical" cause; to fix it, of course, they do not know the cure right now!
In this video we look at the mechanism of death of neurons. Specifically we look at the involvement of the sodium calcium exchange in this.
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Strokes and Excitotoxicity Part 2
Published on Oct 29, 2014In this video we look at the mechanism of death of neurons. Specifically we look at the involvement of the sodium calcium exchange in this.
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Strokes and Excitotoxicity Part 3
Published on Oct 29, 2014In this video we look at the mechanism of death of neurons. Specifically we look at the involvement of the sodium calcium exchange in this.
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Strokes and Excitotoxicity Part 4
Published on Oct 29, 2014In this video we look at the mechanism of death of neurons. Specifically we look at the involvement of the sodium calcium exchange in this.
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Medical Researcher Talks About Evolving Stroke Treatment
Uploaded on Sep 27, 2011Stroke victims may have a longer window of opportunity to receive treatment to save their brain cells, a literature review published by University of Alberta medical researchers in Lancet Neurology demonstrates.
The review, which was published online Sept. 20, was written by Ashfaq Shuaib and his colleagues, including Ken Butcher, an assistant professor of Neurology. Shuaib, the senior author, is a researcher in the Division of Neurology with the Faculty of Medicine & Dentistry. He is also a practising neurologist and a stroke specialist.
Shuaib reviewed stroke studies that examined the use of imaging to measure blood flow in the brain after a stroke. The literature was written from 1980 to July 2011. His review notes that using advanced neuroimaging, such as multi-dimensional brain CT scans and MRIs, can provide physicians important information about blood flow in the brain following a stroke. This information could enable doctors to provide better treatment to prevent brain cells from dying, through the use of techniques to increase blood flow in the brain.
The review noted that the presence of good "collateral" blood flow in the brain can "sustain brain tissue for hours" after major arteries to the brain have been affected by a stroke, and this flow could potentially offset injury to the brain. Enhancing or maintaining strong blood flow is a potential therapeutic treatment for stroke; it is currently under investigation in several stroke centres around the world, says Shuaib.
Normal blood flow in the brain is between 50-60 ml/100g/minute. If someone suffers a stroke and blood-flow levels in the brain fall below 10 ml/100g/minute, brain cells die within minutes of the stroke. However, if blood flow in the brain is between 10-20ml/100g/minute, "the neurons cease function but remain structurally intact and are potentially revivable if normal blood flow is restored," Shuaib says in the review.
He further adds that brain cell death after a stroke may not be complete for hours or even days after a stroke, meaning that the window to treat some stroke patients is longer than three hours—the standard timeframe that has been referenced in medicine since the 1990s. Shuaib says cell death can be complete within as little as an hour in some people following a stroke, while other patients have viable brain tissue and cells for days or indefinitely after a stroke. And with current imaging technology, physicians can determine whether brain cells are dead or have simply ceased functioning post-stroke.
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Excitotoxins, Neurotoxins & Human Neurological Disease Lecture - Dr. Russell Blaylock
Published on May 20, 2013SSTattler: Nice lecture but a little long - about 40 minutes.
Excitotoxins, Neurodegeneration and Neurodevelopment
By Russell L. Blaylock, M.D
There are a growing number of clinicians and basic scientists who are convinced that a group of compounds called excitotoxins play a critical role in the development of several neurological disorders including migraines, seizures, infections, abnormal neural development, certain endocrine disorders, neuropsychiatric disorders, learning disorders in children, AIDS dementia, episodic violence, lyme borreliosis, hepatic encephalopathy, specific types of obesity, and especially the neurodegenerative diseases, such as ALS, Parkinson's disease, Alzheimer's disease, Huntington's disease, and olivopontocerebellar degeneration.
An enormous amount of both clinical and experimental evidence has accumulated over the past decade supporting this basic premise. Yet, the FDA still refuses to recognize the immediate and long term danger to the public caused by the practice of allowing various excitotoxins to be added to the food supply, such as MSG, hydrolyzed vegetable protein, and aspartame. The amount of these neurotoxins added to our food has increased enormously since their first introduction. For example, since 1948 the amount of MSG added to foods has doubled every decade. By 1972 262,000 metric tons were being added to foods. Over 800 million pounds of aspartame have been consumed in various products since it was first approved. Ironically, these food additives have nothing to do with preserving food or protecting its integrity. They are all used to alter the taste of food. MSG, hydrolyzed vegetable protein, and natural flavoring are used to enhance the taste of food so that it taste better. Aspartame is an artificial sweetener.
These toxins (excitotoxins) are not present in just a few foods, but rather in almost all processed foods. In many cases they are being added in disguised forms, such as natural flavoring, spices, yeast extract, textured protein, soy protein extract, etc.
So, what is an excitotoxin? These are substances, usually acidic amino acids that react with specialized receptors in the brain in such a way as to lead to destruction of certain types of neurons. Glutamate is one of the more commonly known excitotoxins. MSG is the sodium salt of glutamate. This amino acid is a normal neurotransmitter in the brain. ...glutamate, as a neurotransmitter, exists in the extracellular fluid only in very, very small concentrations -- no more than 8 to 12uM. When the concentration of this transmitter rises above this level the neurons begin to fire abnormally. At higher concentrations, the cells undergo a specialized process of delayed cell death known as excitotoxicity, that is, they are excited to death.
...in most instances the effects are subtle and develop over a long period of time. While the food additives, MSG and aspartame, are probably not direct causes of the neurodegenerative diseases, such as Alzheimer's dementia, Parkinson's disease, or amyotrophic lateral sclerosis, they may well precipitate these disorders and certainly worsen their pathology as we shall see. It may be that many people with a propensity for developing one of these diseases would never develop a full blown disorder had it not been for their exposure to high levels of food borne excitotoxin additives. Some may have had a very mild form of the disease had it not been for the exposure. Likewise, food borne excitotoxins may be harmful to those suffering from strokes, head injury and HIV infection and certainly should not be used in a hospital setting.
How Excitotoxins Were Discovered
In 1957, two opthalmology residents, Lucas and Newhouse, were conducting an experiment on mice to study a particular eye disorder. During the course of this experiment they fed newborn mice MSG and discovered that all demonstrated widespread destruction of the inner nerve layer of the retina. Similar destruction was also seen in adult mice but not as severe as the newborns.
Then in 1969, Dr. John Olney, a neuroscientist and neuropathologist working out of the Department of Psychiatry at Washington University in St. Louis, repeated Lucas and Newhouse's experiment. His lab assistant noticed that the newborn of MSG exposed mice were grossly obese and short in statue. Further examination also demonstrated hypoplastic organs, including pituitary, thyroid, adrenal as well as reproductive dysfunction. Physiologically, they demonstrated multiple endocrine deficiencies. When Dr. Olney examined the animal's brain, he discovered discrete lesions of the arcuate nucleus as well as less severe destruction of other hypothalamic nuclei. ...We know that when brain cells are injured they release large amounts of glutamate from surrounding astrocytes, and this glutamate can further damage surrounding normal neuronal cells. This appears to be the case in strokes, seizures and brain trauma. But, food born excitotoxins can add significantly to this accumulation of toxins.
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