Imagining the Brain

          Sleep is a very sensitive subject, because too many of us are not getting enough of it.  Despite how hard we try, there seems to not be enough hours in the day to get everything done.  Sometimes the work-load gets so bad that we have to pull all-nighters.
          After not sleeping for a night, someone may find themselves alert and awake.  This seems to be a very bizarre side effect of not resting.  Nora Volkow, MD led a study, which set out to understand this effect.  What she and her team of researchers found was that after a night of no sleep, there is an increase of dopamine in the brain, which helps to keep sleep-deprived subject awake.  The study had test subjects spend a night sleeping or awake, and then took Positron Emission Topography (PET) scans of their brains.
         While this data may seem like an excuse to stay up all night studying, the decreased ability to perform cognition tasks that comes with the dopamine increase is a good reason to make sure you get your 8 hours (or 9.25 if you are in Psych 1101).

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Dopamine Molecule (source: Wikimedia.org)

           Neuroimaging has provided the ability to see inside the living brain and to monitor its structure and function.  From MRI’s, to PET scans, an immense amount of data has been collected to try and find the cause of many neurological, psychiatric and psychological disorders.
           New research has found that MRI scans may be able to predict negative Multiple Sclerosis progression.  Multiple Sclerosis is the breakdown of myelin in the central nervous system.  This leads to reduced muscle coordination, weakness and loss of function.
           At the Brigham and Women’s Hospital and Harvard Medical School, patients with Multiple Sclerosis had their brains scanned using MRI’s.  It was found that those that had “unnatural darkness of gray matter structures” were at a higher risk of disability.
         This study offers hope of understanding the progression of Multiple Sclerosis.  It is also on the cutting edge of neuroimaging use.  Beyond collecting data about disorders, neuroimaging technologies may one day help to identify, and diagnosis disorders.

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           Nowadays, wherever we look, we are surrounded by improvements in technology.  From cell-phones that can access the internet to cars that run on electricity, technology is a consistent part of our lives.  A very important technological advancement may soon be entering our operating rooms.
         In a recent article, there seem to be an advance in robotic technology that can now be used in the operating room. Machines such as neuroArm, and advanced eye tracking systems can now help surgeons perform invasive procedures using small, precise probes and incisions made by robots they were controlling.
         The prospect of robotic surgeries can offer both excitement and distress.  The ability to control movements that are too small for human hands, using a robot would help decrease the chances of excessive bleeding, but the prospect of malfunctions can cause serious consequences.  When assessing the use of robots in the operating room, one must assess both the benefits and the risks that would result from this technology.

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Brain Scan (Getty Images)

Over the past few hundred years, scientists have employed a number of different methods to better understand the intricate workings of the brain.  Brain-scanning technologies are some of the most popular tools currently in use; however, they are misleading because they oversimplify the complexities and subtle realities of the natural world.  While it is true that brain scans have contributed to a better understanding of brain function, it is important to understand their flaws as well.

First off, brain-scanning devices provide an unnatural environment for cognition.  For example, an fMRI machine requires patients to lie completely still in a “coffinesque tube.”  Their heads and bodies are firmly held in place with pads to reduce motion and to get as accurate scans as possible.  This cramped environment induces claustrophobia in as many as 20% of the patients, creating a selection bias.   As a result, the subject sample cannot be truly random, and the fMRI scans do not provide an accurate representation of all brains fairly.

Another flaw is that coloring exaggerates the effects in the brain.  Coloring is used in brain scans to highlight regions with greater neural activity.  Because it is artificial, the process of coloring can easily be manipulated to achieve different results.  For example, the actual difference in activity levels is very small, but scientists can color it and remove all other coloring in the brain scan, creating an exaggerated image.

Furthermore, brain areas activate for various reasons.  The amygdala, a region typically associated with fear, is also activated by positive emotions.  Current technology is not able to separate different processing tasks, so the choice of what to emphasize can be deceptive.

These are just some of the ways that brain scans can be misleading.  While brain-scanning technologies such as fMRI will continue to provide a wealth of information, a better understanding of both its pros and cons will allow people to use that information more effectively.

Read the original article: http://www.sciam.com/article.cfm?id=five-ways-brain-scans-mislead-us

In an attempt to lose weight or maintain their figures, thousands of Americans saunter through their cafeterias and dining halls sporting their favorite diet beverage of choice; however, a new study shows that people who drink diet soft drinks don’t lose weight, in fact, they gain weight.

Sharon P. Fowler, MPH, and his colleagues at the University of Texas Health Science Center, San Antonio, compiled eight years of data relating soft drink consumption to risk of obesity.  While they found that, unsurprisingly, obesity was linked to total soft drink use, they also found that those who only consumed diet soft drinks had a greater risk of obesity than others.

The study consisted of a sampling of over a thousand participants between the ages of 25 and 64.  Of the 622 participants who were of normal weight at the start of the study, roughly one third became overweight or obese after eight years.  The researchers found that, for non-diet soft-drink drinkers, the risk of becoming overweight or obese was roughly 33% for one to two cans of soda consumed a day.  On the other hand, for diet soft-drink drinkers, the risk was roughly 55%.

A possible explanation is that people believe they will lose weight simply by switching from regular to diet sodas, while in reality, a number of different factors results in obesity.

A neurological explanation is that the body craves the calories associated with soda.  If the body senses something that tastes very similar to a lot of calories, it will search for the calories, resulting in a caloric craving.  In a separate study, rat pups fed with artificial sweeteners made them crave more calories than animals fed with real sugar.

Although the study shows that there is some sort of link between diet soda consumption and obesity, Fowler is quick to note that this study does not establish any causal role, rather, they believe that something linked to diet soda consumption is also linked to obesity.

Read the original article: http://www.webmd.com/diet/news/20050613/drink-more-diet-soda-gain-more-weight

It is no secret that many people turn to alcohol after a stressful day at work.  In alcoholics, prolonged alcohol use increases sensitivity to stress, which is a strong trigger for relapse.  Fortunately, a new study shows that blocking a neurotransmitter receptor active in stress also reduces alcohol cravings in people.

Substance P and its receptor neurokinin 1 receptor (NK1R) are the neurotransmitters and receptors involved in fear and anxiety.  Stress has been proven to induce substance P release, and NK1R antagonists have been shown to reduce social anxiety.  Other studies also suggest that NK1R plays a role in drug reward.  Because of its association with both drug reward and stress, the authors of this study wondered whether the receptor mediates stress-associated aspects of alcoholism.

It turns out that a deficiency in NK1R receptors reduces the urge to drink.  In animal studies, NK1R knockout mice consumed less alcohol than did wild-type mice.  Then, after given a sedating dose of alcohol, the knockout mice arose slower than the wild-type mice did.  Similarly, in people, alcoholics tend to be more sensitive to alcohol than occasional drinkers.

In another test, the authors treated a group of alcoholics with an NK1R antagonist that is currently undergoing clinical trials.  The alcoholics were then asked to give a spontaneous speech and do math problems in front of an audience, in an attempt to induce stress.  Meanwhile, the authors showed them alcohol-related cues.  Those who received the antagonist reported fewer stress-induced alcohol cravings than those who received a placebo.

These findings suggest that blocking the NK1R receptor may benefit people who suffer from alcohol abuse.  However, the study only involved subjects who suffered from both alcoholism and anxiety, so the effects of the NK1R receptor on people with different temperaments is still unclear.  Good news for some alcoholics, though, a potential treatment may be right around the corner.

Read the original article: http://www.neuroscience-gateway.org/2008/080403/full/ngw1811.shtml

Chromosome 3 from the Human Genome (life.uiuc.edu)

Researchers at Washington University in St. Louis have found a set of genetic mutations that may have caused cancer (or at least aided in its progression) in a woman in her 50s.  (Cancer is a condition that is caused by uncontrolled growth of cells due to mutations in the cells themselves.)  The mutations were found by studying the donated cells of a patient who died of leukemia while in her 50s.  The experimenters decoded her genes, or mapped her genome.  This makes her the first cancer patient and the first woman to ever have her entire genome decoded.  Two male researchers who completed the “Human Genome Project” mapped their own genomes.

The researchers at Washington University decoded the genes of the patient’s cancerous cells and compared the results to her own genome when mapped from her healthy cells.  They found ten different mutations in the cancer genome that were not present in the healthy genome.  Though this information does not give a definite cause of leukemia, it is definitely a start.  If this sort of detailed information could be obtained for all cancer patients, the similar mutations between them could be discovered.  It is likely that these mutations would be the cancer-causing ones.  If this information could be determined, if the cause of cancer could be discovered, researchers would be well on their way to finding a cure.

Read the original article here.

Researchers at Children’s Hospital Boston may have found a way to treat spinal cord and brain injury.  This is an incredible discovery because there is currently no treatment, due to the fact that injured neurons cannot regenerate.  There is a mechanism in the body that prevents overgrowth of neurons by preventing growth after development has been completed.  Experimenters hypothesized that this mechanism could be regulated within the cells themselves.  The area of neurons that controls cell growth is called the mTOR pathway.  It is active during development but its activities significantly decrease once the cells have matured.  The researchers experimented with this pathway in the brain cells of mice.

Genetic techniques were used to delete two regulators of the mTOR pathway (called PTEN and TSC1), and two weeks later, the optic nerves of the mice were damaged.  Two weeks after that, fifty percent of the injured neurons had survived.  Only twenty percent of the injured neurons survived in the brains of mice who had been subjected to the same optic nerve damage but who had untouched mTOR pathways.  Additionally, ten percent of the mice whose mTOR pathways had been altered showed significant re-growth of the damaged neurons.  This research could lead to the discovery of treatments for spinal cord and brain injuries.  If more experiments are done, a pharmacological way to perform this procedure could be developed, changing the life of many injured patients.

Read the original article here.

In order for a brain to be healthy and to be able to learn and retain information, the proper number of synapses must be present.  Recently, researchers at the Baylor College of Medicine in Houston, Texas, have determined that the protein MeCP2 (methyl-CpG binding protein 2) plays a crucial role in fine-tuning the number of synapses that are in the brain.  They found that too little or too much of this protein could result in mental retardation or symptoms of autism.  This is an extremely significant finding because it could help scientists learn more about what causes autistic disorders.  In fact, one of the researchers suggests that autism could result from a disruption in neuron-to-neuron communication that results from abnormal amounts of MeCP2.  

However, many scientists wondered exactly what the required “perfect” number of synapses would be for the development of a healthy brain.  One of the researchers at the Baylor College of Medicine tackled this question by studying two different sets of mice (one set had too little MeCP2 and one had too much) and asking what was wrong with their neurons.  The question to be answered was whether the neurons themselves were changed depending on the amount of this protein present, or whether the question had more to do with the overall network of neurons and how they communicated with one another.  The results revealed that a loss in MeCP2 caused the neurons to release less neurotransmitters while an increase in MeCP2 caused the opposite, with an increase in communication between neurons and synapses.  Interestingly, the researchers found that the synapses were otherwise functioning normally, which suggests that the development of synaptic connectivity within the brain is tightly regulated by the amount of MeCP2 present.  This is a very powerful piece of evidence that mental retardation and autistic diseases originate with malformation of synapses.  Therefore, once scientists understand more about the implications of MeCP2 in our neurological development, they will begin to understand more about the nature of autism and related neurological disorders.

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A security guard sleeping on the job (Brad and Sabrina - )

These findings are significant in that they may lead scientists to develop more effective therapeutic strategies to alleviate some of the behavioral problems in rotating shift workers.  Such problems include anger, depression, and anxiety, all of which can be explained by low serotonin levels.  In addition, job performance can be improved if these workers received effective help for their “shift work sleep disorders”, which are circadian rhythm sleep disorders that occur due to a work schedule that takes place during the normal sleep period.  This type of disorder can cause the workers to have trouble sleeping or to be severely tired, which can cause them to be less alert and put them at risk of an injury on the job.

Sleep disorders associated with shift work can affect male and female workers of all age groups, and estimates are that two to five percent of the general population is affected.  Now that the problem has been explained by decreased levels of serotonin, new treatments may be on the way which are specifically targeted at these shift workers.

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