The Brain What Happens to a Linebacker's Neurons?
A blow to the head can change the neural architecture of the brain from elastic to brittle, with devastating consequences.
by Carl ZimmerFrom the July-August special issue; published online August 18, 2010
These kinks form, Smith believes, when microtubules are stretched so rapidly that they snap. The broken filaments can no longer slide neatly back over one another and instead bunch up, causing the kinks. Normally, enzymes inside neurons are constantly taking apart microtubules and building new ones with the recycled parts. But now the enzymes attack the broken ends of the microtubules, causing the internal structure of the axon to dissolve. With the microtubules turning to mush, the axon begins to relax and lose its kinks. The axons look fairly normal, but they are catastrophically damaged.
Microtubules do more than give neurons their structure. They also serve as a kind of cellular railway network. Proteins travel from one end of a neuron to the other by moving along microtubules. If microtubules break, the result is much like what happens when a railroad track is damaged. The proteins pile up, and these traffic jams produce the swellings in the axons that Smith sees in his experiments. The swellings get so big that they eventually rupture, tearing the axon apart and spewing out damaged proteins.
Smith’s findings could shed light on a common but puzzling brain trauma known as diffuse axonal injury. This happens when people experience sudden accelerations to the brain—from a bomb’s shock waves, for example, or from whiplash in a car crash. Very often the acceleration causes people to lose consciousness. In serious cases it can lead to trouble with cognitive tasks, such as deciding whether the word red is actually printed in red. When pathologists perform autopsies on people with diffuse axonal injury, they see severed axons with swollen tips, just like what Smith sees in his experiments.
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Smith’s research also suggests that even mild shocks to the brain can cause serious harm. If he hit his axons with gentle puffs of air, they didn’t swell and break. Nevertheless, there was a major change in their molecular structure. Axons create the electric current that allows them to send signals by drawing in positively charged sodium ions*. A moderate stretch to an axon, Smith recently found, causes the sodium channels to malfunction. In order to keep the current flowing, the traumatized axons start to build more channels.
Smith suspects that such a mended axon may be able to go on working, but only in a very frail state. Another stretch—even a moderate one—can cause the axon to go haywire. Its additional sodium channels now malfunction, and the axon tries to compensate by creating even more channels. But these channels are now so defective that they start letting in positively charged calcium ions. The calcium atoms activate enzymes that destroy the gates that slow the flow of sodium through the channels, so now even more sodium rushes in—and then more calcium, in a runaway feedback loop. The axon dies like a shorted-out circuit.
This slower type of axon death may happen when someone suffers mild but repeated brain injuries, exactly the kind that football players experience as they crash into each other in game after game. Cognitive tests like the ones at this year’s N.F.L. combine can pinpoint the mental troubles that come with dysfunctional or dying axons. There is precious little research to indicate how long a football player should be sidelined in order to let his brain recover, though, and Smith’s experiments don’t offer much comfort. Preliminary brain studies show that axons are still vulnerable even months after an initial stretch.
Once a person does sustain a brain injury, there is not a lot doctors can do. They can open a hole in the skull if pressure in the brain gets too high. But they have no drugs to treat the actual damage. Some 30 compounds have made it into phase 3 trials in humans, only to fail.
The latest research could point scientists to more effective treatments. Smith, for example, recently found that the anticancer drug taxol can stabilize the microtubules in neurons, protecting them from catastrophic disassembly after a sharp shock. Now that we know the damage to the brain happens at the molecular level, we may find a cure for the injured brain waiting there as well.
* Correction, August 23, 2010: This sentence originally referred to "negatively charged sodium atoms."
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Great explanation on how the brain is damaged. This occurs in car accident whiplash injuries on a regular basis. Even mild rear end collisions can cause brain trauma and neck injury.
I take Resveratrol every day to help with cognitive function and to decrease inflammation. This with B vitamins is a great way to decrease your chances of Alzheimers.
From EWG Report
The Environmental Working Group (EWG) has released results of the most extensive tests to date of cancer-causing polychlorinated biphenyl (PCBs) levels in farmed salmon consumed in the United States. EWG bought the salmon from local grocery stores and found seven of 10 fish were so contaminated with PCBs that they raise cancer-risk concerns, relative to health standards of the US Environmental Protection Agency (EPA).
Salmon farming has made salmon the third most popular fish in America
and comprises 22 percent of all retail seafood counter sales. However, EWG analysis of government data also found that farmed salmon are likely the most PCB-contaminated protein source in the current U.S. food supply.
EWG analysis of state-of-the-art fish consumption data derived from 20,000 adults from 1990 through 2002 shows that roughly 800,000 US adults are 100 times over their lifetime allowable cancer risk by eating this contaminated salmon.
PCBs were banned in the U.S. in the late 1970s and are among the dirty dozen chemical contaminants slated for global phase-out under the UN treaty on persistent organic pollutants. PCBs are highly persistent, and they have been linked to cancer and impaired fetal brain development.
Farmed salmon are fattened with ground fishmeal and fish oils that are high in PCBs. As a result, salmon farming operations that produce inexpensive fish unnaturally concentrate PCBs and have a higher fat content. Farmed salmon contains 52 percent more fat than wild salmon, according to USDA data.
Wild Alaskan salmon eat Pacific Ocean fish that are naturally lower in persistent pollutants, and they carry less fat than farmed salmon.
The Food and Drug Administration (FDA), which has control over store-bought fish, uses PCB safety standards set in 1984. For recreationally caught fish, the EPA employs a more recent standard that reflects current scientific concerns about PCBs and is 500 times safer than the FDA’s.
FDA could not have predicted the rise of the farmed salmon industry when it set its PCB safety standard decades ago, said EWG Vice President for Research Jane Houlihan. The industrys growth has been rapid and unexpected, but it is having a real public health consequence.
EWG called for more resources to be given to the FDA so it can move quickly to conduct a study of PCB contamination in farmed salmon – and make all the results public. This testing is critical, because FDA will be unable to act to lower public exposure to PCBs in farmed salmon until they conduct these studies. Congress should also pass a funding increase for FDA to support this testing.
In the meantime, EWG recommends that consumers choose wild instead of farmed salmon, and they should eat an eight-ounce serving of farmed salmon no more than once a month. Consumers should also trim fat from the fish before cooking – and choose broiling, baking, or grilling over frying, as these cooking methods allow the PCB-laden fat to cook off the fish.
Wild salmon dominated the market just ten years ago. Now, six of every 10 salmon fillets sold in stores and restaurants are from fish raised in high-density pens in the ocean, managed and marketed by the salmon farming industry. Before salmon farming, PCB exposure was declining, but the trend is now being reversed due to farmed fish.
When Congress banned PCBs in 1976, no one contemplated that 20-odd years later we would have invented a new industry that re-concentrates these toxins in our bodies, said Houlihan.
Dr. Perlmutter’s comment:
To my readers, please note that this was published back in 2003. Nonetheless, it is still critically important information and I would urge you to visit the link.
At the end of the article they try to minimize the danger of wearing this patch by saying most of the clots haven't caused any deaths. Could that be do to just plain luck? If this were a vitamin supplement it would be on the front page of every news paper and the FDA would have pulled it off the market in a heart beat.
Revisiting Lynam's notion of the "fledgling psychopath": are HIA-CP children truly psychopathic-like? Michonski, Jared D Sharp, Carla info:doi/10.1186/1753-2000-4-24 info:pmid/20815906 Child and Adolescent Psychiatry and Mental Health 2010, 4:24 2010-09-03 Child and Adolescent Psychiatry and Mental Health 2010-09-03 4 1 Research 24 -->Research
Revisiting Lynam's notion of the "fledgling psychopath": are HIA-CP children truly psychopathic-like?
Jared D Michonski
and Carla Sharp
Department of Psychology, 126 Heyne Building, Houston, Texas, 77204, USA
author email
corresponding author email
Child and Adolescent Psychiatry and Mental Health 2010, 4:24doi:10.1186/1753-2000-4-24
The electronic version of this article is the complete one and can be found online at: http://www.capmh.com/content/4/1/24
Received: 28 June 2010 Accepted: 3 September 2010 Published: 3 September 2010 © 2010 Michonski and Sharp; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
