Signs And Symptoms Of Brain Problems

Brains are very complex organs. Each day we depend on them to help us do the simplest things such as brushing our teeth to solving the most complex problems, like whether to apply for a new job or not. There are certain injuries and sicknesses that can stop the brain from functioning the way it used to or the way others do.

The first kind of brain problem that can occur is caused by trauma. This can be a impact of the head of any kind from mild to severe. Head trauma can cause skull fractures, hematoma and contusions of the brain tissue. Where and how hard you are hit will partly determine the extent of the damage of the brain injury.

Headaches are also a type of brain problem or symptom. These can range from simple headaches to more painful headaches such as migraines. If you are finding your headaches are more frequent or longer lasting it is possible it is pointing to some bigger problem with your overall brain health.

One of the most serious brain injuries that can occur is a brain aneurysm. An aneurysm is a weak blood vessel in the brain. If this aneurysm bursts before you get to a medical professional it could be potentially fatal. The usual symptoms are a terrible headache that comes on quickly you could also experience double vision, neck stiffness and eye pain.

Another serious medical condition that can product brain symptoms is a stroke. A stroke can occur when the brain is temporarily deprived of oxygen which can be caused from a few different reasons. Strokes can have lasting effects in some cases including headaches, confusion memory loss or paralysis.

Although some brain traumas such as headaches are simple and will go away on their own there are some symptoms that require immediate medical treatment. These symptoms include change in consciousness, change in mental status such as hallucinations or lethargy, double vision, difficulty walking, garbled speech, loss of muscle use and severe stiff necks or headaches. If you experience any of these symptoms it is best to dial emergency right away.

Keeping the brain in optimal condition is essential to your overall brain health. If you suspect you may have a brain injury or are experiencing any of these symptoms you should consider getting checked by a doctor as soon as possible. The sooner you find out the problem the less likely you are to experience long term brain issues.

Nathanael Eisenberg is the CEO of CogniFit, a company that develops software which measure and train cognitive abilities. We help people discover new insights about themselves and decide what to improve in their life.

The rapid growth of scientific knowledge around the brain creates new opportunities to help tackle some of the major challenges of the early part of the 21st century. Nathanael's goal is to participate in the search of some of these additional solutions.

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5 Lifestyle Tips To Help Your Brain

These Lifestyle Tips Could Help Save Your Brain

Research has shown that there are a number of activities that can be incorporated into your lifestyle that can prevent cognitive and physical decline. Adopting some simple daily habits, and doing them regularly, as well as paying closer attention to the ones you do anyway, will result in both cognitive and physical health, as you get older.

1 Reduce your stress

Extensive research has highlighted the negative effects that stress has on both your body and your brain. The worst kind of stress that the brain can experience, and which leads to brain damage if it continues unchecked, is stress that combines these three factors:

A lack of predictabilityA lack of controlA lack of obvious outlets for the resultant frustration

Hints to reduce this type of stress:

Learn to live in the moment. Simply take a deep breath and focus on the moment that you find yourself in. Plan for the future, but don't live in it.Identify the stresses that are most likely to make you to feel as if you have no control. Accept or avoid what you can't change.Talk to someone who has had a similar challenge.Learn to say NO! You will be amazed how this one factor can transform your life.Do some 'de-junking' to reduce stress - it is easier to handle stress when you are organized.Move on from the past - whatever it takes - forgiveness, counseling, acceptance.Make a point of listing the things that you are grateful for at the end of each day. This lowers depression, which is a risk factor for cognitive decline.Extending yourself, through volunteering. This reduces both stress and depression.Laugh regularly. Happy people laugh, and are less likely to suffer from depression and stress.Foster strong, positive relationships, which support cognitive health. Move away from ones that leave you felling frustrated and unhappy.Exercise is a natural de-stressor, using up the chemicals that are produced when you feel stressed, overwhelmed and frustrated.

2 Exercise your body to help your brain

Research has indicated clearly that exercise strengthens the brain, through strengthening the heart firstly, but also through a direct mechanism that actually influences neurons. Exercise benefits your brain in the following ways:

Your heart works harder and becomes stronger by pumping more blood and oxygen around your body and into your brain when you exercise. More blood, and more oxygen and nutrients being pumped throughout your body, mean more gets to your brain too.Exercising helps your blood vessels stay strong and healthy, which is protective against burst blood vessels in the brain.More blood being pumped into the brain means an increase in the growth of specific cells, called astrocytes, that support neurons.Exercise lowers your risk of getting heart disease, depression, diabetes, or experiencing hypertension, which - combined, or separately - are all risk factors for brain dysfunction and the death of neurons.

Further reasons why exercise benefits your brain starts deep within your muscles when you exercise:

Chemicals produced in working muscles, find their way into the brain, increasing the production of a chemical, called Brain Derived Neurotrophic Factor, or BDNF, which acts like fertilizer for your neurons, encouraging them to stay healthy and keep growing, even helping to grow new neurons.Exercising regularly, your brain builds up reserves of BDNF, helping neurons to branch out, joining together, forming new connections.A mood disorder may be a 'lack of movement' disorder, as specific neurotransmitters are increased after exercising, which give you a feeling of being happy and calm, focused and less impulsive.Your brain becomes more and more efficient at producing BDNF the more you exercise.An increased blood flow to the brain decreases inflammation.

3 Sleep enough to keep your brain sharp

Your body evolved to spend a third of its life asleep - less than that and you end up with a problem. There are a few very unusual people who seem to need less sleep, but researchers believe this is an exception to the sleep needs of most people. We get ill and eventually die when we are severely sleep deprived. These are some of the reasons why this may happen, and why the brain is severely affected by sleep deprivation:

Your blood pressure drops when you sleep, which is good for your heartDreaming seems to perform important functions in your brain, even though researchers do not yet understand this fullyA number of hormones are released when you sleep, three of which are very important in the process of healing and rejuvenation that occurs during sleep:Erythropoietin is produced in your kidneys, during deep sleep, to stimulate red blood cell production in your bone marrow.Growth hormone is a special hormone produced in your pituitary gland at regular intervals of about 90 minutes, during sleep. The most powerful wave occurs about an hour after you fall asleep at night.Testosterone is an important hormone, for both men and women, ensuring high levels of energy, a healthy libido, good immunity against illness and strong bones. Poor sleep leads to low levels of testosterone.Rat brains, deprived of sleep, experience more neuronal damage due to oxidation, from energy production within neurons. Sleep seems to allow the production of antioxidant-like compounds, which counteract the damage that occurs during the day. The hippocampus, the memory centre, is the area that seems to be affected most severely when sleep deprivation occurs. Humans seem to experience the same negative effects from sleep deprivation.Further research into sleep-deprived rats has found that their brains accumulate Amyloid-beta, a form of protein that is involved in Alzheimer's disease. Research has yet to uncover whether this is true for humans too, but it seems wise to err on the side of caution, and get enough sleep.

4 Mental stimulation will keep your brain young

Researchers have discovered that being socially active, engaging in many activities that involve relating to others, and being involved in new experiences, uses your brain and keeps it active. This mental activity is now believed to be very important in keeping your brain healthy, and also helps your neurons to generate new connections.

There are a few specific pointers to keep in mind when making choices about how to keep your brain stimulated:

The more educated a person is, the greater their ability to withstand age-related cognitive decline. This is called 'cognitive reserve.' However it is never too late to learn new things, so don't let not receiving a qualification in your youth stop you from pursuing further education now.Do a few things differently, every day, to stimulate new pathways in your brain, like, going to work via a different route, using your non-dominant hand for daily tasks and eating with chopsticks.Learn new things by having in depth discussions with people who are experts in their fields.Spark new interests, new thoughts and new discussions by reading different books to what you have become used to reading.Researchers believe that playing chess and sudoka, while fun and mildly stimulating, doesn't really make long term changes to the structure of the brain, so should not be relied on to provide all the mental stimulation that your brain needs as it gets older.Go somewhere new on holiday, where you will encounter a new culture and even a new language, once again increasing neuronal connections, and therefore cognitive health.Specific computer games can stimulate the release of specific chemicals within the brain, which can foster long term, positive, neuronal change.

5 Watch your weight to keep your brain healthy

As you get older, weight gain can be an insidious, creeping enemy, and a lack of physical exercise will increase the problem. People who are overweight are more likely to experience cardiovascular disease, type 2 diabetes and depression, all of which are predisposing factors for mental illness and cognitive decline.

Research has also indicated that increasing body mass index (BMI) coupled with increasing age is associated with decreased brain volume, helping to explain decreased cognitive ability.

The over-consumption of refined carbohydrates, a low consumption of nutrient dense fresh produce, combined with an impaired digestive system, which often accompanies aging, and a lack of the correct Essential Fatty Acids, will all lead to weight gain, and general ill health, both mentally and physically.

Furthermore, impaired glucose sensitivity, which occurs due to the excessive intake of refined carbohydrates, and which is a pre-cursor for diabetes, is also linked to diminished cognitive ability. People who have good glucose control hold onto their memories for longer, than people who have impaired glucose sensitivity.

In conclusion, normal aging, added to unmanageable stress levels, inactivity, poor sleep, little mental stimulation and a negative outlook on life, accompanied by slow, but significant weight gain, will magnify cognitive decline. By keeping an open mind and an open heart, you are open to new experiences and by default will be open to ongoing brain stimulation, and good cognitive health.

Delia McCabe is a Nutritional Neuroscience Researcher. She has a Masters degree in Psychology and has been doing research for over ten years. Her specific area of interest is Essential Fatty Acids and how they effect brain and general health. She has discovered that many chronic illnesses and mental health problems can be traced back to a lack of Essential Fats. Find out if you are deficient by doing the quick assessment at http://www.deliahealth.com/.

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Understanding The Effect Of Stress On The Brain

When one is under stress, the brain sends nerve signals to the adrenal glands to facilitate the release of adrenaline. Adrenaline will then increase the blood sugar, increase the heart rate and the blood pressure, among other actions. Apart from that, hypothalamus will facilitate the pituitary gland to stimulate the production of Cortisol from the adrenal cortex. Cortisol is a stress hormone that helps in an individual's response to stress, as it keeps the blood sugar and blood pressure high to help them get away from the danger.

This is the normal reaction the brain undergoes when under stress in the short term, but it is extremely damaging in case it goes on for a long time. The main reason for this is that the increasing amount of Cortisol will reduce the effectiveness of the immune system and affect the memory because it decreases the number of brain cells.

In research, it has been indicated that Cortisol damages and kills cells in the part of the brain that is responsible for short-term memory - the hippocampus. This makes the brain unable to access existing memory or forming a new one. At the same time it interferes with neurotransmitters, the chemicals that facilitate communication between brain cells. As a result many people are unable to retrieve a long term memory when in a crisis and are unable to think clearly. The reason why working memory is lost in stressful conditions is the fact that the stress hormones divert glucose to the exercising muscles, causing a lower amount of energy to reach the hippocampus. Consequently, it impedes us to create new memory. This is the reason why many people do not remember traumatic events, and why the working memory is usually the first to 'get lost'.

It is also known to be a cause of premature aging of the brain. When Cortisol is released in the brain, it binds different neurons in the cytoplasm. After a series of reactions, the neurons release more calcium. In case calcium increases in the brain, the neurons will fire faster and more frequently and eventually die. Further research has also indicated that there might be a connection between changes in the ippocampus and Alzheimer's disease. Some experts explain that the shrinkage and damage of specific parts of the hippocampus affect specific memory abilities and the higher the shrinkage the faster the individuals will progress towards Alzheimer's.

For this reason, it is important for people to try to avoid stress in order to have a healthy brain. The best way to do this is to take charge of their thoughts and emotions so that they can handle different situations better, without compromising the brain fitness. Individuals can also engage in relaxing activities to reduce the stress levels as well as keep their sharp minds. They can also opt for meditation or deep breathing in order to free the mind from stress and bring about a calming sensation. In so doing, they will drastically reduce the amount of Cortisol in the brain, allowing them to salvage their memory and focus to keep a healthy brain.

View the original article here ezine.com

10 Food Tips To Help Your Brain

Simple Food Habits To Help You Preserve Your Precious Brain

Although the brain is such a complex organ, determining who we are, and how we navigate our way through this world, its maintenance and care doesn't have to be complicated. Just keep these basic facts in mind:

Your brain loves fat

60% of your brain is made up of fat, so the kind of fat that you need to consume has to be of a very high quality. Your brain is especially fond of Omega 3 fats, but also needs Omega 6's. These essential fats are very delicate and prone to damage, so you need to consume an undamaged blend.

Your brain loves water

The largest component in your body is water, so you need to consume enough clean, uncontaminated water to keep your body and brain well hydrated.

Your brain loves protein

Protein is important, not just for building muscle, but also for keeping your neurons talking effectively. If you don't eat enough good quality protein, your neurons battle to chat to each other, and you could find it difficult to concentrate, leading to memory challenges. Protein should be organic, if it comes from an animal, and you need to combine grains with legumes to make complete protein, if you are a vegetarian.

Your brain is the greediest organ in your body

Your brain is the most energy hungry organ in your body. It needs a constant, stable supply of good quality carbohydrates. Vegetables and low-sugar fruit provide good, fresh sources of carbohydrates, for sustained energy production, while processed and refined carbohydrates provide short-term energy fixes. Choose whole grains and legumes for sustained energy release too, and your brain will enjoy optimal energy supply. A wide variety of fresh produce will also supply vitamins and minerals that your brain needs to function optimally.

Your brain on coffee

Caffeine supplies a quick rush of energy to your brain, because it stimulates the release of adrenaline. This makes you feel energetic to start with, but soon tapers off, leaving you in need of another 'fix.' Try one of the great herbal teas available, or opt for plain old-fashioned water, with a dash of lime. Most people don't need another stress kick, and this is exactly what coffee provides.

Your brain needs the right carbohydrates

Think of what you crave. If it is chocolate and lollies, you are probably experiencing unstable glucose levels, because of processed carbohydrate consumption, so you have to wean yourself from these insidious addictions. When people are tired, from lack of sleep, ongoing stress and feeling overwhelmed, they usually reach for a quick-sugar-fix to give them a spurt of energy. A great green drink, full of nutrient rich compounds, can help to get your blood glucose more stable, and lead to less cravings. Eating the right fats helps immensely too, because your cells produce energy more efficiently with the right fats, keeping your energy levels high, which leads to less energy slumps, and chocolate-fixes.

What goes on in your gut will effect what goes on between your ears

Contrary to popular belief, you aren't what you eat - you are what you absorb. This means that you need to sort out any digestive difficulties you may be experiencing. Your food needs to be digested, absorbed and waste eliminated effectively, before you can be optimally healthy. Your brain can only receive the nutrients that are absorbed, so it makes perfect sense to ensure your gut is working well.

If your body doesn't like a food, your brain will object too

If you are intolerant to any food, such as wheat or dairy, your brain can battle to stay alert and focused. This will of course affect your memory negatively. Researchers are still working on exactly why food intolerance affects the brain so negatively, but if you suspect you may be intolerant to a specific food, leave it out of your diet for a couple of weeks, and see how you feel. Interestingly, the foods that you crave are often the ones that don't agree with you, as they produce an addictive-like response in your body. So, if you think you can't live without it, the chances are your body - and brain - can do with out it.

Food additives don't add up to better brain function

Check the labels of the food that you are eating. If you eat lots of fresh produce, there are no labels, but there are additives in tinned and processed foods, that may be causing harm to your body and brain. Many additives are simply present in the product to make the product shelf-stable, and ensure no loss of income for the manufacturer. Furthermore, some additives are actively dangerous, like MSG, which is an excitotoxin, causing neuron damage, and eventually loss, when consumed in excess.

Eat breakfast like a king to keep your brain happy throughout the day

Whether you have breakfast doesn't just determine your weight, it also determines how your brain will work during the day. When people miss breakfast they are setting themselves up for weight gain, because they tend to eat more during the day. Furthermore, focus, memory and mood are all influenced negatively by a lack of breakfast. If you are not hungry when you wake up, consider taking your breakfast with you. As it's best to eat only after you've been awake for about an hour, it may pay you to prepare your breakfast, and eat it when you arrive at your destination. It sure beats a cup of coffee and a muffin at your desk. Otherwise, you can go to bed earlier, and then wake up in time to exercise, and then eat your breakfast.

These tips may take some time to implement, but even changing only one to start with, is a move in the right direction.

Delia McCabe is a Nutritional Neuroscience Researcher. She has a Masters degree in Psychology and has been doing research for over ten years. Her specific area of interest is Essential Fatty Acids and how they effect brain and general health. She has discovered that many chronic illnesses and mental health problems can be traced back to a lack of Essential Fats. Find out if you are deficient by doing the quick assessment at http://www.deliahealth.com/.

View the original article here ezine.com

Nicotine can protect the brain from Parkinson's disease, research suggests

ScienceDaily (Aug. 1, 2011) — If you've ever wondered if nicotine offered society any benefit, a new study published in The FASEB Journal offers a surprising answer. Nicotine can protect the brain against Parkinson's disease, the research suggests, and the discovery of how nicotine does this may lead to entirely new types of treatments for the disease.

"This study raises the hope for a possible neuroprotective treatment of patients at an early step of the disease or even before at a stage where the disease has not been diagnosed according to motor criteria," said Patrick P. Michel, co-author of the study from the Institut du Cerveau et de la Moelle Épinière, Hôpital de la Salpêtrière, in Paris, France.

To make this discovery, scientists used mice genetically engineered without a specific nicotine receptor (the alpha-7 subtype) and mice with a functional receptor. Using tissue from mouse embryos, researchers prepared brain cultures using conditions that favor the slowly progressing loss of dopamine neurons, a hallmark of the disease. The scientists found that nicotine had the potential to rescue dopamine neurons in cultures from normal mice, but not in cultures from mice without the nicotine receptor. These findings suggest that it may be feasible to develop novel therapies for Parkinson's disease that target nicotine receptors, particularly the alpha-7 nicotine receptor.

"If you're a smoker, don't get too excited," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "Even if smoking protects you from Parkinson's, you might not live long enough to develop the disease because smoking greatly increases the risk for deadly cancers and cardiovascular diseases. But now, we should be able find non-toxic ways to hit the same target."

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Federation of American Societies for Experimental Biology, via EurekAlert!, a service of AAAS.

Journal Reference:

D. Toulorge, S. Guerreiro, A. Hild, U. Maskos, E. C. Hirsch, P. P. Michel. Neuroprotection of midbrain dopamine neurons by nicotine is gated by cytoplasmic Ca2. The FASEB Journal, 2011; 25 (8): 2563 DOI: 10.1096/fj.11-182824

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here sciencedaily.com

Non-invasive brain stimulation helps curb impulsivity

ScienceDaily (June 15, 2011) — Inhibitory control can be boosted with a mild form of brain stimulation, according to a study published in the June 2011 issue of Neuroimage. The study's findings indicate that non-invasive intervention can greatly improve patients' inhibitory control. Conducted by a research team led by Dr Chi-Hung Juan of the Institute of Cognitive Neuroscience, National Central University in Taiwan, the research was sponsored by the National Science Council in Taiwan, the UK Medical Research Council, the Royal Society Wolfson Merit Award, and a Fulbright Award.

The study demonstrates that when a weak electrical current is applied over the front of participants' scalps for ten minutes, it greatly improved their ability to process responses -- effectively jumpstarting the brain's ability to control impulsivity. The treatment has the potential to serve as a non invasive treatment for patients with conditions such as attention-deficit hyperactivity disorder (ADHD), Tourette's syndrome, drug addictions, or violent impulsivity.

Professor Chi-Hung Juan who led the research team noted, "The findings that electrical stimulation to the brain can improve control of their behavioral urges not only provide further understanding of the neural basis of inhibitory control but also suggest a possible therapeutic intervention method for clinical populations, such as those with drug additions or ADHD, in the future."

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Elsevier, via AlphaGalileo.

Journal Reference:

Tzu-Yu Hsu, Lin-Yuan Tseng, Jia-Xin Yu, Wen-Jui Kuo, Daisy L. Hung, Ovid J.L. Tzeng, Vincent Walsh, Neil G. Muggleton, Chi-Hung Juan. Modulating inhibitory control with direct current stimulation of the superior medial frontal cortex. NeuroImage, 2011; DOI: 10.1016/j.neuroimage.2011.03.059

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here sciencedaily.com

High blood pressure, diabetes, smoking and obesity in middle age may shrink brain, damage thinking

ScienceDaily (Aug. 2, 2011) — A new study suggests smoking, high blood pressure, diabetes and being overweight in middle age may cause brain shrinkage and lead to cognitive problems up to a decade later. The study is published in the August 2, 2011, print issue of Neurology®, the medical journal of the American Academy of Neurology.

"These factors appeared to cause the brain to lose volume, to develop lesions secondary to presumed vascular injury, and also appeared to affect its ability to plan and make decisions as quickly as 10 years later. A different pattern of association was observed for each of the factors," said study author Charles DeCarli, MD, with the University of California at Davis in Sacramento and a Fellow of the American Academy of Neurology. "Our findings provide evidence that identifying these risk factors early in people of middle age could be useful in screening people for at-risk dementia and encouraging people to make changes to their lifestyle before it's too late."

The study involved 1,352 people without dementia from the Framingham Offspring Study with an average age of 54.

Participants had body mass and waist circumference measures taken and were given blood pressure, cholesterol and diabetes tests. They also underwent brain MRI scans over the span of a decade, the first starting about seven years after the initial risk factor exam. Participants with stroke and dementia at baseline were excluded, and between the first and last MRI exams, 19 people had a stroke and two developed dementia.

The study found that people with high blood pressure developed white matter hyperintensities, or small areas of vascular brain damage, at a faster rate than those with normal blood pressure readings and had a more rapid worsening of scores on tests of executive function, or planning and decision making, corresponding to five and eight years of chronological aging respectively.

People with diabetes in middle age lost brain volume in the hippocampus (measured indirectly using a surrogate marker) at a faster rate than those without diabetes. Smokers lost brain volume overall and in the hippocampus at a faster rate than nonsmokers and were also more likely to have a rapid increase in white matter hyperintensities.

People who were obese at middle age were more likely to be in the top 25 percent of those with the faster rate of decline in scores on tests of executive function, DeCarli said. People with a high waist-to-hip ratio were more likely to be in the top 25 percent of those with faster decrease in their brain volume.

The study was supported by the National Heart, Lung, and Blood Institute, the National Institute of Neurological Disorders and Stroke and the National Institute on Aging.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Academy of Neurology.

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here sciencedaily.com

Risk factors predictive of psychiatric symptoms after traumatic brain injury

ScienceDaily (July 11, 2011) — A history of psychiatric illness such as depression or anxiety before a traumatic brain injury (TBI), together with other risk factors, are strongly predictive of post-TBI psychiatric disorders, according to an article published in Journal of Neurotrauma, a peer-reviewed journal published by Mary Ann Liebert, Inc.

In addition to a pre-injury psychiatric disorder, two other factors are early indicators of an increased risk for psychiatric illness one year after a TBI: psychiatric symptoms during the acute post-injury period, and a concurrent limb injury. Kate Rachel Gould, DPsych, Jennie Louise Ponsford, PhD, Lisa Johnston, PhD, and Michael Schönberger, PhD, Epworth Hospital and Monash University, Melbourne, Australia, and University of Freiburg, Baden-Württemberg, Germany, also describe a link between risk of psychiatric symptoms and unemployment, pain, and poor quality of life during the 12-month post-TBI period.

In the presence of a limb injury, patients who suffered a TBI had a 6.4 greater risk of psychiatric disorders at 1 year, and a 4-fold greater risk of depression in particular, compared to patients without a limb injury.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Mary Ann Liebert, Inc., via EurekAlert!, a service of AAAS.

Journal Reference:

Kate Rachel Gould, Jennie Louise Ponsford, Lisa Johnston, Michael Schönberger. Predictive and Associated Factors of Psychiatric Disorders after Traumatic Brain Injury: A Prospective Study. Journal of Neurotrauma, 2011; : 110613150039035 DOI: 10.1089/neu.2010.1528

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here sciencedaily.com

Stress in the city: Brain activity and biology behind mood disorders of urbanites

ScienceDaily (June 23, 2011) — Being born and raised in a major urban area is associated with greater lifetime risk for anxiety and mood disorders. Until now, the biology for these associations had not been described. A new international study, which involved Douglas Mental Health University Institute researcher Jens Pruessner, is the first to show that two distinct brain regions that regulate emotion and stress are affected by city living. These findings, published in Nature may lead to strategies that improve the quality of life for city dwellers.

"Previous findings have shown that the risk for anxiety disorders is 21 percent higher for people from the city, who also have a 39 percent increase for mood disorders," says co-author Jens Pruessner, a Douglas researcher. "In addition, the incidence for schizophrenia is almost doubled for individuals who are born and brought up in cities. These values are a cause for concern and determining the biology behind this is the first step to remedy the trend."

Distinct brain structures

Pruessner, with his colleagues from the Central Institute of Mental Health in Mannheim, looked at the brain activity of healthy volunteers from urban and rural areas. In a series of functional magnetic resonance experiments involving the Douglas' previously developed 'Montreal Imaging Stress Task',(MIST) protocol, they showed that city living was associated with greater stress responses in the amygdala, an area of the brain involved with emotional regulation and mood. In contrast, urban upbringing was found to be associated with activity in the cingulate cortex, a region involved in regulation of negative affect and stress.

"These findings suggest that different brain regions are sensitive to the experience of city living during different times across the lifespan," says Pruessner. "Future studies need to clarify the link between psychopathology and these affects in individuals with mental disorders.These findings contribute to our understanding of urban environmental risk for mental disorders and health in general. They further point to a new approach to interface social sciences, neurosciences and public policy to respond to the major health challenge of urbanization."

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Douglas Mental Health University Institute.

Journal Reference:

Florian Lederbogen, Peter Kirsch, Leila Haddad, Fabian Streit, Heike Tost, Philipp Schuch, Stefan Wüst, Jens C. Pruessner, Marcella Rietschel, Michael Deuschle, Andreas Meyer-Lindenberg. City living and urban upbringing affect neural social stress processing in humans. Nature, 2011; 474 (7352): 498 DOI: 10.1038/nature10190

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here sciencedaily.com

Newly developed molecule tested as a delivery vehicle to image and kill brain tumors

ScienceDaily (Aug. 3, 2011) — A single compound with dual function -- the ability to deliver a diagnostic and therapeutic agent -- may one day be used to enhance the diagnosis, imaging and treatment of brain tumors, according to findings from Virginia Commonwealth University and Virginia Tech.

Glioblastomas are the most common and aggressive brain tumor in humans, with a high rate of relapse. These tumor cells often extend beyond the well-defined tumor margins making it extremely difficult for clinicians and radiologists to visualize with current imaging techniques. Researchers have been investigating enhanced methods of attacking these cells in order to possibly delay or prevent brain tumor relapse.

In a study published in the August issue of the journal Radiology, the research team led by Panos Fatouros, Ph.D., a former professor and chair of the Division of Radiation Physics and Biology in the VCU School of Medicine who retired in 2010, demonstrated that a nanoparticle containing an MRI diagnostic agent can effectively be imaged within the brain tumor and provide radiation therapy in an animal model.

The nanoparticle filled with gadolinium, a sensitive MRI contrast agent for imaging, and coupled with radioactive lutetium 177 to deliver brachytherapy, is known as a theranostic agent -- a single compound capable of delivering simultaneously effective treatment and imaging. The lutetium 177 is attached to the outside of the carbon cage of the nanoparticle.

"We believe the clustering properties of this nanoplatform prolong its retention within the tumor, thereby allowing a higher radiation dose to be delivered locally," said Michael Shultz, Ph.D., a research fellow in Fatouros' lab in the Department of Radiology in the VCU School of Medicine.

"This theranostic agent could potentially provide critical data about tumor response to therapy by means of longitudinal imaging without further contrast administration," said Fatouros.

A nanoparticle called a functionalized metallofullerene (fMF), also known as a "buckyball," served as the basis of this work and was created by study collaborator, Harry Dorn, Ph.D., a chemistry professor at Virginia Tech, and his team. In 1999, Dorn and his colleagues were able to encapsulate rare earth metals in the hollow interior of these nanoparticles that can easily be recognized by MRI techniques.

"Although this is a limited animal study, it shows great promise and hopefully this metallofullerene platform will be extended to humans," said Dorn.

Fatouros, who is the corresponding author on the study, Shultz and Dorn collaborated with John D. Wilson, Ph.D., associate professor in the VCU Department of Radiology; Christine E. Fuller, M.D., professor and director of neuropathology and autopsy pathology at VCU; and Jianyuan "Jason" Zhang, a graduate student in chemistry at Virginia Tech from Beijing, China.

The study was funded by grants to Fatouros from the National Institutes of Health's National Cancer Institute, and to Dorn from the National Science Foundation.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Virginia Commonwealth University.

Journal Reference:

John D. Wilson, Christine E. Fuller, Jianyuan Zhang, Harry C. Dorn, Panos P. Fatouros. Metallofullerene-based Nanoplatform for Brain Tumor Brachytherapy and Longitudinal Imaging in a Murine Orthotopic Xenograft Model. Radiology, 2011; DOI: 10.1148/radiol.11102569

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

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Have we met before? Scientists show why the brain has the answer

ScienceDaily (Aug. 4, 2011) — Have you ever been approached by someone whose face you recognize but whose name you can't remember? Neuroscientists at the University of Bristol have identified the reasons behind why we are, at times, unable to link a face to a name.

The research, led by Dr Clea Warburton and Dr Gareth Barker in the University's School of Physiology and Pharmacology and published in the Journal of Neuroscience, has investigated why we can recognise faces much better if we have extra clues as to where or indeed when we encountered them in the first place.

The study found that when we need to remember that a particular object, for example a face, occurred in a particular place, or at a particular time, multiple brain regions have to work together -- not independently.

It has been known for some time that three brain regions appear to have specific roles in memory processing. The perirhinal cortex seems to be critical for our ability to recognise whether an individual object is novel or familiar, the hippocampus is important for recognising places and for navigation, while the medial prefrontal cortex is associated with higher brain functions.

These most recent studies, however, are the first to look at situations where these brain regions interact all together, rather than considering each one individually.

Dr Warburton said: "We are very excited to discover this important brain circuit. We're now studying how memory information is processed within it, in the hope we can then understand how our own 'internal library' system works."

The researchers investigated the neural basis of our ability to recognise different types of stimuli under different conditions. Of specific interest were two types of recognition memory: 'object-in-place recognition memory' (remembering where we put our keys), and 'temporal order recognition memory' (when we last had them).

Neither 'object-in-place' or 'temporal order recognition' memories could be formed if communication between the hippocampus and either the perirhinal cortex, or the medial prefrontal cortex, was broken. In other words, disconnecting the regions prevented the ability to remember both where objects had been, and in which order.

Finding that these regions must all act together has important implications for understanding memory and helping treat people with memory disorders such as Alzheimer's disease.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Bristol, via EurekAlert!, a service of AAAS.

Journal Reference:

G. R. I. Barker, E. C. Warburton. When Is the Hippocampus Involved in Recognition Memory? Journal of Neuroscience, 2011; 31 (29): 10721 DOI: 10.1523/JNEUROSCI.6413-10.2011

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Long periods of estrogen deprivation jeopardizes brain receptors, stroke protection

ScienceDaily (Aug. 2, 2011) — Prolonged estrogen deprivation in aging rats dramatically reduces the number of brain receptors for the hormone as well as its ability to prevent strokes, researchers report.

However the damage is forestalled if estrogen replacement begins shortly after hormone levels drop, according to a study published in the journal Proceedings of the National Academy of Sciences.

"This is further evidence of a critical window for estrogen therapy, either right before or right after menopause," said Dr. Darrell W. Brann, Chief of GHSU's Developmental Neurobiology Program and the study's corresponding author.

The surprising results of the much-publicized Women's Health Initiative -- a 12-year study of 161,808 women ages 50-79 -- found hormone therapy generally increased rather than decreased stroke risk as well as other health problems. Critics said one problem with the study was that many of the women, like Brann's aged rats, had gone years without hormone replacement, bolstering the case that timing is everything.

Brann's earlier work in the hippocampus, a center for cognition, learning and memory, also showed a reduction in hormone receptors in younger rodents that were models of surgical menopause but left questions about why the loss occurred and whether it occurred naturally with aging. The new study documents that loss as unused receptors become targets for elimination in rats mimicking 60-65 year olds, about a decade past menopause. Interestingly, the receptor loss did not occur in the uterus, which remained sensitive to estrogen.

After long periods without estrogen, researchers found that an enzyme called CHIP -- carboxyl terminus of Hsc70 interacting protein -- increased binding with estrogen receptor alpha, a major brain receptor for neuroprotection. While CHIP levels remain unchanged, the increased binding results in about half the receptors getting hauled to the cell's proteosome to be chopped up and degraded. "We think this is the mechanism for how the receptor gets degraded," Brann said.

When researchers later treated the aged rats with estrogen, they found what the Women's Health Initiative showed: increased mortality. "So it did not seem to do anything good and maybe it did some harm in older rats and that is similar to what the WHI found," Brann said. The brain protection afforded by estrogen when given earlier to the rats, suggested the "critical window." Additionally when CHIP activity was blocked, so was the receptor destruction.

Next steps include estrogen-treating those rats where CHIP-related destruction is blocked to see if salvaged receptors will respond and looking at the process in other areas of the brain.

"We think the estrogen receptor decrease is why the sensitivity decreases," said Brann, who also is Associate Director of GHSU's Institute of Molecular Medicine and Genetics. "If the hormone is gone long enough it is logical there would be decreased sensitivity as normal feedback between the receptor and hormone is reduced."

Collaborators include scientists at Hebei United University in China and the University of Texas Health Sciences Center at San Antonio. Dr. Quan-guang Zhang, Research Scientist in Brann's lab, is the study's first author. Aged rats were obtained from the National Institute on Aging and studies were funded by the National Institutes of Health and American Heart Association.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Georgia Health Sciences University.

Journal Reference:

Q.-g. Zhang, D. Han, R.-m. Wang, Y. Dong, F. Yang, R. K. Vadlamudi, D. W. Brann. PNAS Plus: C terminus of Hsc70-interacting protein (CHIP)-mediated degradation of hippocampal estrogen receptor-  and the critical period hypothesis of estrogen neuroprotection. Proceedings of the National Academy of Sciences, 2011; DOI: 10.1073/pnas.1104391108

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Scary driving? Put the brakes on using your brain power

ScienceDaily (July 29, 2011) — German researchers have used drivers' brain signals, for the first time, to assist in braking, providing much quicker reaction times and a potential solution to the thousands of car accidents that are caused by human error.

Using electroencephalography (EEG) -- a technique that attaches electrodes to the scalp -, the researchers demonstrated that the mind-reading system, accompanied with modern traffic sensors, could detect a driver's intention to break 130 milliseconds faster than a normal brake pedal response.

Driving at 100km/h, this amounts to reducing the braking distance by 3.66 meters -- the full length of a compact car or the potential margin between causing and avoiding accidents.

The study, published the 29th of July 2011, in IOP Publishing's Journal of Neural Engineering, identified the parts of the brain that are most active when braking and used a driving simulator to demonstrate the viability of mind-reading assisted driving.

As well as EEG, the researchers, from the Berlin Institute for Technology, also chose to examine myoelectric (EMG) activity which is caused by muscle tension in the lower leg and can be used to detect leg motion before it actually moves to the brake pedal.

Whilst sat among conventional driving controls, the study's 18 participants were asked to drive a car that was displayed on a screen in front of them whilst a series of electrodes were attached to their scalp to measure brain activity.

They were asked to stay within a 20 metre distance of a computer-controlled lead vehicle along a road that contained sharp curves and dense oncoming traffic, to recreate real driving conditions, whilst maintaining a speed of 100km/h.

At random intervals, emergency braking situations were triggered by the rapid braking of the lead vehicle in front, accompanied by the flashing of its braking lights.

At this point, when the subjects reacted, the data was collected from the EEG and EMG. For comparison, the researchers also recorded information on the time it took to release the gas pedal and press the brake pedal, the deceleration of both vehicles and the distance between the two vehicles.

Using the initial EEG recordings, the researchers were able to determine what parts of the brain are most sensitive in a braking scenario and therefore tweak the detection system accordingly.

A recent development, implemented into this study, are hybrid systems where external lasers and sensors are able to sense when a potential crash is upcoming so that as soon as the break pedal is touched, the vehicles goes into an emergency braking procedure; however these systems still rely on a human physical response, which is where a mind-reading system could benefit.

Lead author of the study Stefan Haufe said, "Averaged over all potential detection thresholds, a system that uses all available sensors detects emergency situations 130 milliseconds earlier than a system that doesn't use EEG and EMG. We can safely say that it is mainly EEG that leads to the early detection.

"We are now considering to test the system online in a real car however if such a technology would ever enter a commercial product, it would certainly be used to complement other assistive technology to avoid the consequences of false alarms that could be both annoying and dangerous."

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Institute of Physics, via EurekAlert!, a service of AAAS.

Journal Reference:

Stefan Haufe, Matthias S Treder, Manfred F Gugler, Max Sagebaum, Gabriel Curio and Benjamin Blankertz. EEG potentials predict upcoming emergency brakings during simulated driving. Journal of Neural Engineering, Volume 8 Number 5 DOI: 10.1088/1741-2560/8/5/056001

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Children and adolescent cell phone users at no greater risk of brain cancer than non-users, study suggests

ScienceDaily (July 28, 2011) — Children and adolescents who use mobile phones are not at a statistically significant increased risk of brain cancer compared to their peers who do not use mobile phones, according to a study published July 27 in the Journal of The National Cancer Institute.

Mobile phone usage has increased among children and adolescents in recent years. The increased usage has raised a concern about the possibility of the development of brain tumors in this population since children have a developing nervous system; also, because their head circumference is smaller, the radio frequency electromagnetic fields may penetrate regions that are deeper in their brains. However, no previous study has examined whether mobile phone usage among children and adolescents is associated with a difference in brain tumor risk.

To determine the relationship between mobile phone usage and brain tumor risk among children and adolescents, Martin Röösli, Ph.D, of the Swiss Tropical and Public Health Institute in Basel, Switzerland, and colleagues looked at the medical records of children aged 7-19 with brain tumors, identified through population registries. Researchers did face-to-face interviews with them regarding their mobile phone usage. They also consulted data from phone network providers.

The study, conducted between 2004 and 2008, included participants from Norway, Denmark, Sweden and Switzerland. They looked at data for 352 brain cancer patients, and 646 control subjects.

The researchers found that patients with brain tumors were not statistically significantly more likely to have been regular mobile phone users than control subjects. They found that 265 (75.3%) of case patients and 466 control subjects (72.1%) reported having spoken on a mobile phone more than 20 times before the time when the case patient was diagnosed. Furthermore, 194 case patients (55%) and 329 control subjects (51%) reported regular mobile phone usage. However, in a subset of study participants for whom operator recorded data were available, brain tumor risk was related to the time elapsed since the mobile phone subscription was started (but not to amount of use). No increased risk of brain tumors was observed for brain areas receiving the highest amount of exposure.

The researchers write, "Because we did not find a clear exposure-response relationship in most of these analyses, the available evidence does not support a causal association between the use of mobile phones and brain tumors." Nevertheless, since mobile phone usage among children and adolescents has increased over the years, they encourage a careful watch on the trend.

In an accompanying editorial, John D Boice, Jr., ScD. and Robert E. Tarone, PhD., of the International Epidemiology Institute in Rockville, Maryland and Vanderbilt University in Nashville, Tennessee write that Röösli and his colleagues "have filled an important gap in knowledge by showing no increased risk of brain tumors among children and adolescents who are regular cell phone users"

Boice and Tarone conclude that it is reassuring that the incidence rates of brain cancer in the general population, including children and teenagers, have not changed over the past 20 years in the United States and many other countries despite the steady and marked rise in the use of cell phones throughout the world since the 1980s. They recommend that investigators continue to monitor population incidence rates and that in the meantime, individuals who are concerned might consider alternatives to holding a cell phone up to their ears, such as using an ear piece or using the phone's speaker. They also point out that individuals should heed what is known about real risks by avoiding the use of cell phones while driving a car, because such distractions have been clearly documented to increase the risk of accidents and injuries.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Journal of the National Cancer Institute, via EurekAlert!, a service of AAAS.

Journal References:

John D. Boice, Jr and Robert E. Tarone. Cell Phones, Cancer, and Children. J Natl Cancer Inst, July 27, 2011 DOI: 10.1093/jnci/djr285Denis Aydin, Maria Feychting, Joachim Schüz, Tore Tynes, Tina Veje Andersen, Lisbeth Samsø Schmidt, Aslak Harbo Poulsen, Christoffer Johansen, Michaela Prochazka, Birgitta Lannering, Lars Klæboe, Tone Eggen, Daniela Jenni, Michael Grotzer, Nicolas Von der Weid, Claudia E. Kuehni, and Martin Röösli. Mobile Phone Use and Brain Tumors in Children and Adolescents: A Multicenter Case–Control Study. J Natl Cancer Inst, July 27, 2011 DOI: 10.1093/jnci/djr244

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Aging brains are different in humans and chimpanzees; Evolution of human longevity led to both a large brain and brain shrinkage

ScienceDaily (July 29, 2011) — Brains shrink in humans, potentially causing a number of health problems and mental illnesses as people age, but do they shrink to the same extent in the closest living relatives to humans--the chimpanzees?

New research says no, making the extreme amount of brain shrinkage resulting from normal aging in humans unique.

Chet Sherwood, an anthropologist at The George Washington University in Washington, D.C., and a team of scientists from seven other U.S. universities put forward the question to see if comparable data on the effects of aging could be found in chimpanzees. Such data on regional brain volumes in chimpanzees was not available, until now.

The researchers -- anthropologists, neuroscientists, psychologists, biologists, and veterinary professionals -- used magnetic resonance imaging (MRI) to measure the space occupied by various brain structures in adult humans and chimpanzees, including the frontal lobe and the hippocampus, an area of the brain associated with short-term and long-term memory.

They found chimpanzees do not display significant loss, or atrophy, in the size of their brains and other internal structures as they age.

Instead, Sherwood and colleagues suggest that as humans evolved the ability to live longer, the result was a "high degree of brain degeneration" as people get older.

"We were most surprised that chimpanzees, who are separated from humans by only 6-8 million years of independent evolution, did not more closely resemble the human pattern of brain aging," said Sherwood. "It was already known that macaque monkeys, separated from humans by about 30 million years, do not show humanlike, widespread brain atrophy in aging."

The current issue of Proceedings of the National Academy of Sciences reports the findings. The National Science Foundation (NSF) partially funded the research.

Because humans and chimpanzees grow, develop and age on different schedules, the study compared humans from age 22 to 88 and chimpanzees from age 10 to 51. For both species, this encompassed the whole adult lifespan under natural conditions. Humans have a longer lifespan than chimpanzees. In the wild, the lifespan of chimpanzees is about 45 at the oldest. With medical care in captivity, they can live into their 60s. On the other hand, humans without access to modern medical care and who live in traditional hunter-gatherer societies can live to their mid-80s.

The researchers used MRI to measure the volume of the whole brain, total neocortical gray matter, total neocortical white matter, frontal lobe gray matter, frontal lobe white matter and the hippocampus in a cross-sectional sample of 99 chimpanzees and 87 adult humans.

"Traits that distinguish humans from other primates include enlargement of the brain and increased longevity," they write in the report "Aging of the Cerebral Cortex Differs Between Humans and Chimpanzees."

Consequently, they say, humans are unique among animals in being susceptible to certain neuropathologies, such as Alzheimer's disease, in the later stages of life. Even in the absence of disease, however, healthy aging in humans is marked by variable degrees of neural deterioration and cognitive impairment.

"This is an excellent example of research that has implications for societal benefits," said NSF Physical Anthropology Program Officer Kaye Reed. "While Dr. Sherwood and colleagues are interested in the evolutionary significance of brain differences between chimpanzees and humans, the results of this research can be used as a basis to explore degenerative brain diseases, such as Alzheimer's, in a medical context."

"This research points to the uniqueness of how severe brain aging is in humans," said Sherwood. "While there are certainly many similarities between humans and other animals in the degenerative processes that occur in the brain, our research indicates that even healthy, normal aging in humans involves more pronounced brain deterioration than in other species.

"Taken together with particular environmental and genetic risk factors, this might help to explain the fact that only humans are vulnerable to developing dementing illnesses like Alzheimer's disease in old age."

Sherwood and colleagues conclude evolution led to both a large brain and a long lifespan in humans. They point out that the benefits of these traits are much debated, but they surmise it might be related to an increased reliance on social learning of skills.

"As a result, we suggest that the high energy cost of a large brain in humans leads to more wear and tear that cannot be easily repaired because most neurons are not renewed," said Sherwood. "As a consequence, human brains become more vulnerable to degeneration towards the later stages of life."

In addition to NSF, the National Institutes of Health, the James S. McDonnell Foundation, the Mathers Foundation and a Yerkes Center Grant supported the research.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by National Science Foundation.

Journal Reference:

C. C. Sherwood, A. D. Gordon, J. S. Allen, K. A. Phillips, J. M. Erwin, P. R. Hof, W. D. Hopkins. Aging of the cerebral cortex differs between humans and chimpanzees. Proceedings of the National Academy of Sciences, 2011; DOI: 10.1073/pnas.1016709108

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Mouse with 'off switch' in key brain cell population developed; Research may increase understanding of SIDS, depressive disorders

ScienceDaily (July 30, 2011) — NIH-funded scientists have developed a strain of mice with a built-in off switch that can selectively shut down the animals' serotonin-producing cells, which make up a brain network controlling breathing, temperature regulation, and mood. The switch controls only the serotonin-producing cells, and does not affect any other cells in the animal's brains or bodies.

When the researchers powered down the animals' serotonin cells, the animals failed to sufficiently step up their breathing to compensate for an increase of carbon dioxide in the air, and their body temperatures dropped to match the surrounding temperature.

The finding has implications for understanding sudden infant death syndrome, or SIDS, which has been linked to low serotonin levels, and is thought to involve breathing abnormalities and problems with temperature control. The finding may also provide insight into depressive disorders, which also involve serotonin metabolism.

The study results appear in the current issue of the journal Science.

SIDS is the death of an infant before his or her first birthday that cannot be explained after a complete autopsy, an investigation of the scene and circumstances of the death, and a review of the medical history of the infant and of his or her family. According to the National Center for Health Statistics, SIDS is the third leading cause of infant death.

"The single most effective way to reduce the risk of SIDS is to always place infants on their backs for sleep," said Marian Willinger, Ph.D., special assistant for SIDS at the NIH's Eunice Kennedy Shriver National Institute of Child Health and Human Development, which provided major funding for the study. "This new animal model of the serotonin-producing system holds the promise of helping us to understand the biological processes contributing to SIDS, which is critical for the development of tests and interventions to prevent these deaths.'' Additional NIH support was provided by the National Institute of Mental Health, National Institute on Drug Abuse, and National Center for Research Resources.

To conduct the study, the researchers developed mice with a unique molecule, or receptor, on the surface of their serotonin-producing brain cells, or neurons. Typically, cells communicate via chemicals that bind to receptors on their surfaces, with the molecules binding to their receptors in much the same way a key fits into a lock.

The researchers added this special receptor to the animal's serotonin-producing neurons using a genetic manipulation technique they developed called intersectional genetics. The special receptor was developed by NIH-funded researcher Bryan Roth. The approach consists of manipulating the animals' genetic material so that it manufacturers an additional receptor on the surface of its neurons. In this case, the animals' serotonin-producing cells began making a receptor that is not found in nature. Rather than binding to a naturally occurring brain chemical, the receptor binds to a chemical compound manufactured in a laboratory, clozapine-N-oxide (CNO).

"CNO was identified for its ability to bind specifically to this foreign receptor that we placed into the serotonin cells, and because it does not react with other cells or tissues in the animal's body," Dr. Dymecki explained.

When CNO binds with the receptor, it deactivates only the serotonin cells, effectively switching off all communications in the serotonin network. CNO does not affect any other cells in the animals' brains or bodies.

"By selectively switching off the serotonin-producing cells, we can get a definite idea of what bodily functions the serotonin cells specifically control" she said.

The researchers exposed genetically normal mice and mice with the receptor for CNO to elevated levels of carbon dioxide. Carbon dioxide is the waste product given off when a breath is exhaled. If carbon dioxide builds up in the body, due to insufficient breathing, it can be toxic, leading to loss of consciousness and death. The response to high carbon dioxide accumulation is increased breathing and a faster breathing rate, which releases carbon dioxide through the lungs.

When the normal mice were exposed to carbon dioxide, they almost immediately began to breathe faster and more deeply. In contrast, after their serotonin-producing neurons were switched off, mice with the receptor to CNO had a smaller response to carbon dioxide and did not increase their breathing as much.

"This finding shows that the breathing response to carbon dioxide is regulated by serotonin neurons," Dr. Dymecki said.

The researchers next tested the ability of the CNO-responsive mice to regulate their body temperatures. When the room temperature was set at 74 degrees Fahrenheit, the body temperature of normal mice remained at about 98.6 degrees -- the normal temperature for mice. Normal mice can maintain a normal body temperature even when the room temperature is cool and below that of body temperature, Dr. Dymecki added. However, after their serotonin neurons were switched off with CNO, the body temperatures of the CNO mice soon plunged. Like reptiles faced with a sudden temperature drop, the body temperatures of the mice soon dropped to the 74 degree room temperature.

"Their body temperatures were equilibrating with the room temperature," Dr. Dymecki said. "Our finding affirms that temperature is regulated by the serotonergic system."

Dr. Dymecki explained that the researchers added the CNO receptor to all the animals' serotonergic neurons. In future studies, she and her colleagues plan to selectively add the receptor to subsets of serotonergic receptors, to better understand their functioning in health, and in disorders such as SIDS and depression.

The finding provides support for previous autopsy studies by NIH grantees implicating abnormalities in serotonin metabolism in the brainstem as playing a role in SIDS.

Researchers theorize that infants who die of SIDS may have been unable to respond to breathing challenges, such as low levels of oxygen or high levels of carbon dioxide. High levels of carbon dioxide may accumulate around the face of an infant sleeping face down, when the infant's exhaled breath accumulates in a pocket formed by bedding materials.

The ability to regulate body temperature is also thought to play a role in SIDS deaths. The NICHD's Back to Sleep campaign advises parents and caregivers to avoid letting infants overheat during sleep, to dress them in light sleep clothes, avoid blankets or coverings, and to keep the room at a temperature that is comfortable for an adult.

Other authors of the paper were Russell Ray and Rachael Brust, also of the Department of Genetics at Harvard Medical School; Andrea Corcoran and Eugene Nattie, Department of Physiology at Dartmouth Medical School, in Lebanon, N.H.; Jun Chul Kim, Department of Psychology, University of Toronto, Toronto, Ontario, Canada; and George B. Richerson, Department of Neurology, University of Iowa in Iowa City.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by NIH/National Institute of Child Health and Human Development.

Journal Reference:

R. S. Ray, A. E. Corcoran, R. D. Brust, J. C. Kim, G. B. Richerson, E. Nattie, S. M. Dymecki. Impaired Respiratory and Body Temperature Control Upon Acute Serotonergic Neuron Inhibition. Science, 2011; 333 (6042): 637 DOI: 10.1126/science.1205295

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Eliminating protein in specific brain cells blocks nicotine reward

ScienceDaily (July 27, 2011) — Removing a protein from cells located in the brain's reward center blocks the anxiety-reducing and rewarding effects of nicotine, according to a new animal study in the July 27 issue of The Journal of Neuroscience. The findings may help researchers better understand how nicotine affects the brain.

Nicotine works by binding to proteins called nicotinic receptors on the surface of brain cells. In the new study, researchers led by Tresa McGranahan, Stephen Heinemann, PhD, and T. K. Booker, PhD, of the Salk Institute for Biological Studies, found that removing a specific type of nicotinic receptor from brain cells that produce dopamine -- a chemical released in response to reward -- makes mice less likely to seek out nicotine. The mice also did not show reductions in anxiety-like behaviors normally seen after nicotine treatment. Smokers commonly report anxiety relief as a key factor in continued smoking or relapse.

"These findings show that the rewarding and anxiety-reducing properties of nicotine, thought to play a key role in the development of tobacco addiction, are related to actions at a single set of brain cells," said Paul Kenny, PhD, an expert on drug addiction at Scripps Research Institute, who was unaffiliated with the study.

Previous studies showed blocking the alpha4 nicotinic receptor within the ventral tegmental area (VTA) -- a brain region important in motivation, emotion, and addiction -- decreases the rewarding properties of nicotine. Because alpha4 receptors are present on several cell types in the VTA, it was unclear how nicotine produced pleasurable feelings.

To zero in on the circuit important in the brain's response to nicotine, researchers developed mice with a mutation that left them unable to produce the alpha4 receptor, but only on dopamine brain cells. Mice lacking alpha4 receptors in these cells spent less time looking to obtain nicotine compared with normal mice, suggesting the alpha4 receptors are required for the rewarding effects of nicotine. Nicotine also failed to reduce anxiety-like behaviors in the mutant mice, as it normally does in healthy mice.

"Identification of the type of nicotinic receptors necessary for two key features of nicotine addiction -- reward and anxiety -- may help us better understand the pathway that leads to nicotine dependence, and potential treatment for the one billion cigarette smokers worldwide," McGranahan said. Diseases from tobacco use remain a major killer throughout the world, causing more than 5 million deaths per year.

The findings could guide researchers to a better understanding of the mechanisms of tobacco addiction and assist in the development of new drugs to treat tobacco addiction and provide relief from anxiety disorders, Kenny added.

The research was supported by the National Institute of Neurological Disorders and Stroke, the National Institute on Alcohol Abuse and Alcoholism, and the National Institute on Drug Abuse.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Society for Neuroscience, via EurekAlert!, a service of AAAS.

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How the brain keeps track of what we're doing

ScienceDaily (July 29, 2011) — "Working memory" is what we have to keep track of things moment to moment: driving on a highway and focusing on the vehicles around us, then forgetting them as we move on; remembering all the names at the dinner party while conversing with one person about her job.

Most psychologists explain working memory with a "controlled attention" model: one flexible system that directs the brain's focus to stimuli and tasks that are important and suppressing the rest. The capacity of working memory, they say, is limited by our ability to attend to only one thing at a time.

Now, in the August issue of Current Directions in Psychological Science, a journal published by the Association for Psychological Science, University of Edinburgh cognitive neuroscientist Robert H. Logie challenges this model.

"We have a range of different capacities, each with its own function, and they operate at the same time" when we perform a task or think about something, says Logie. Within this "multiple-component framework," working memory capacity is "the sum of the capacities of all these different functions."

This "workspace" in the brain, as Logie calls it, allows us to do something while other functions operate in the background or to apply ourselves to a single task involving more than one function. In reading, for instance, we both see words and process meaning. The "sum" of the capacities isn't a gross measure, though, because we often tax one function more than another. In reading, processing has its shoulder to the grindstone, while vision takes it easy.

In addition to the attentional model of working memory, Logie critiques the experimental methods shaped by it. Example: Studies measuring capacity ask participants to read a sentence (process) and remember the sentence's last word (memory), then read several sentences and recall all the final words in order. How well a person does can predict performance on other tasks or exams. But the experiment, which assumes one big resource pouring into different tasks until it's used up, tests only one function, memory for words.

If you want to understand not just the capacity but the structure of working memory -- which Logie considers a more fruitful avenue of research -- there's a better experimental methodology: cognitive neuroscience. "Imaging data demonstrate that if you ask people to do one sort of task, you get one [brain] pattern, and if you ask them to do another, you get another pattern." Make the same task harder -- say, remember word lists faster -- and "you see increased activation in the same area." Complicate it -- add words to the sequence, and thus processing along with recall -- and different networks fire.

The multiple-component model holds great practical promise, says Logie. In education, "if you assume there is a single general capacity," interventions for people struggling to learn are few. Assume multiple components to draw on, and those other resources stand ready for development.

Similarly, if you see general impairment in aging or after brain damage, you can give only generalized support. Look for decline or impairment in specific functions -- not just physical but cognitive -- and you can exercise the still-robust functions, helping people live richer, more independent lives.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Association for Psychological Science.

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Traumatic brain injury linked with tenfold increase in stroke risk

ScienceDaily (July 29, 2011) — If you suffer traumatic brain injury, your risk of having a stroke within three months may increase tenfold, according to a new study reported in Stroke: Journal of the American Heart Association.

"It's reasonable to assume that cerebrovascular damage in the head caused by a traumatic brain injury can trigger either a hemorrhagic stroke [when a blood vessel bursts inside the brain] or an ischemic stroke [when an artery in the brain is blocked]," said Herng-Ching Lin, Ph.D., senior study author and professor at the School of Health Care Administration, College of Medicine, Taipei Medical University in Taiwan. "However, until now, no research had been done showing a correlation between traumatic brain injury and stroke."

It is the first study that pinpoints traumatic brain injury as a potential risk factor for subsequent stroke.

Traumatic brain injury occurs when an external force such as a bump, blow or jolt to the head disrupts the normal function of the brain. Causes include falls, vehicle accidents, and violence.

In the United States alone, approximately 1 in 53 individuals sustain a traumatic brain injury each year, according to 2004 statistics from the Centers for Disease Control and Prevention.

Worldwide, traumatic brain injuries are a major cause of physical impairment, social disruption and death.

Using records from a nationwide Taiwanese database, researchers investigated the risk of stroke in traumatic brain injury patients during a five-year period. The records included 23,199 adult traumatic brain injury patients who received ambulatory or hospital care between 2001 and 2003. The comparison group comprised 69,597 non-traumatic brain injury patients. The average age of all patients was 42 and 54 percent were male.

During the three months after injury, 2.91 percent of traumatic brain injury patients suffered a stroke compared with only 0.30 percent of those with non-traumatic brain injury -- a tenfold difference.

Stroke risk in patients with traumatic brain injury decreased gradually over time, researchers said:

After one year, the risk was about 4.6 times greater for patients who suffered a traumatic brain injury than for those who had not.After five years, the risk was 2.3 times greater for traumatic brain injury patients.

Stroke risk among traumatic brain injury patients with skull bone fractures was more pronounced than in traumatic brain injury patients without fractures, researchers said.

During the first three months, those with skull bone fractures were 20 times more likely to have a stroke than patients without skull bone fractures. The risk decreased over time.

Furthermore, the risk of subarachnoid hemorrhage (bleeding in the area between the brain and the thin tissues that cover the brain) and intracerebral hemorrhage (bleeding in the brain caused by the rupture of a blood vessel) increased significantly in patients with traumatic brain injury versus non-traumatic brain injury patients.

After considering age and gender, patients with traumatic brain injury were more likely to have hypertension, diabetes, coronary heart disease, atrial fibrillation and heart failure than non-traumatic brain injury patients.

Early neuroimaging examinations -- such as MRI -- and intensive medical monitoring, support and intervention should be required following a traumatic brain injury, especially during the first few months and years, Lin said. Moreover, better health education initiatives could increase public awareness about the factors that cause strokes and the signs and symptoms of stroke in patients with traumatic brain injuries.

"Stroke is the most serious and disabling neurological disorder worldwide," said Lin. "Our study leads the way in identifying stroke as an additional neurological problem that may arise following traumatic brain injury."

Co-authors are: Yi-Hua-Chen, Ph.D, lead author and Jiunn-Horng Kang, M.D.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Heart Association, via EurekAlert!, a service of AAAS.

Journal Reference:

Y.-H. Chen, J.-H. Kang, H.-C. Lin. Patients With Traumatic Brain Injury: Population-Based Study Suggests Increased Risk of Stroke. Stroke, 2011; DOI: 10.1161/STROKEAHA.111.620112

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

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'Brain cap' technology turns thought into motion; Mind-machine interface could lead to new life-changing technologies for millions of people

ScienceDaily (July 29, 2011) — "Brain cap" technology being developed at the University of Maryland allows users to turn their thoughts into motion. Associate Professor of Kinesiology José 'Pepe' L. Contreras-Vidal and his team have created a non-invasive, sensor-lined cap with neural interface software that soon could be used to control computers, robotic prosthetic limbs, motorized wheelchairs and even digital avatars.

"We are on track to develop, test and make available to the public- within the next few years -- a safe, reliable, noninvasive brain computer interface that can bring life-changing technology to millions of people whose ability to move has been diminished due to paralysis, stroke or other injury or illness," said Contreras-Vidal of the university's School of Public Health.

The potential and rapid progression of the UMD brain cap technology can be seen in a host of recent developments, including a just published study in the Journal of Neurophysiology, new grants from the National Science Foundation (NSF) and National Institutes of Health, and a growing list of partners that includes the University of Maryland School of Medicine, the Veterans Affairs Maryland Health Care System, the Johns Hopkins University Applied Physics Laboratory, Rice University and Walter Reed Army Medical Center's Integrated Department of Orthopaedics & Rehabilitation.

"We are doing something that few previously thought was possible," said Contreras-Vidal, who is also an affiliate professor in Maryland's Fischell Department of Bioengineering and the university's Neuroscience and Cognitive Science Program. "We use EEG [electroencephalography] to non-invasively read brain waves and translate them into movement commands for computers and other devices.

Peer Reviewed

Contreras-Vidal and his team have published three major papers on their technology over the past 18 months, the latest a just released study in the Journal of Neurophysiology in which they successfully used EEG brain signals to reconstruct the complex 3-D movements of the ankle, knee and hip joints during human treadmill walking. In two earlier studies they showed (1) similar results for 3-D hand movement and (2) that subjects wearing the brain cap could control a computer cursor with their thoughts.

Alessandro Presacco, a second-year doctoral student in Contreras-Vidal's Neural Engineering and Smart Prosthetics Lab, Contreras-Vidal and co-authors write that their Journal of Neurophysiology study indicated "that EEG signals can be used to study the cortical dynamics of walking and to develop brain-machine interfaces aimed at restoring human gait function."

There are other brain computer interface technologies under development, but Contreras-Vidal notes that these competing technologies are either very invasive, requiring electrodes to be implanted directly in the brain, or, if noninvasive, require much more training to use than does UMD's EEG-based, brain cap technology.

Partnering to Help Sufferers of Injury and Stroke

Contreras-Vidal and his team are collaborating on a rapidly growing cadre projects with researchers at other institutions to develop thought-controlled robotic prosthetics that can assist victims of injury and stroke. Their latest partnership is supported by a new $1.2 million NSF grant. Under this grant, Contreras-Vidal's Maryland team is embarking on a four-year project with researchers at Rice University, the University of Michigan and Drexel University to design a prosthetic arm that amputees can control directly with their brains, and which will allow users to feel what their robotic arm touches.

"There's nothing fictional about this," said Rice University co-principal investigator Marcia O'Malley, an associate professor of mechanical engineering. "The investigators on this grant have already demonstrated that much of this is possible. What remains is to bring all of it -- non-invasive neural decoding, direct brain control and [touch] sensory feedback -- together into one device."

In a NIH-supported project underway, Contreras-Vidal and his colleagues are pairing their brain cap's EEG-based technology with a DARPA-funded next-generation robotic arm designed by researchers at the Johns Hopkins Applied Physics Laboratory to function like a normal limb. And the UMD team is developing a new collaboration with the New Zealand's start-up Rexbionics, the developer of a powered lower-limb exoskeleton called Rex that could be used to restore gait after spinal cord injury.

Two of the earliest partnerships formed by Contreras-Vidal and his team are with the University of Maryland School of Medicine in Baltimore and the Veterans Affairs Medical Center in Baltimore. A particular focus of this research is the use of the brain cap technology to help stroke victims whose brain injuries affect their motor-sensory control. Originally funded by a seed grant from the University of Maryland, College Park and the University of Maryland, Baltimore, the work now also is supported by a VA merit grant (anklebot BMI) and an NIH grant (Stroke).

"There is a big push in brain science to understand what exercise does in terms of motor learning or motor retraining of the human brain," says Larry Forrester, an associate professor of physical therapy and rehabilitation science at the University of Maryland School of Medicine.

For the more than a year, Forrester and the UMD team have tracked the neural activity of people on a treadmill doing precise tasks like stepping over dotted lines. The researchers are matching specific brain activity recorded in real time with exact lower-limb movements.

This data could help stroke victims in several ways, Forrester says. One is a prosthetic device, called an "anklebot," or ankle robot, that stores data from a normal human gait and assists partially paralyzed people. People who are less mobile commonly suffer from other health issues such as obesity, diabetes or cardiovascular problems, Forrester says, "so we want to get [stroke survivors] up and moving by whatever means possible."

The second use of the EEG data in stroke victims is more complex, yet offers exciting possibilities. "By decoding the motion of a normal gait," Contreras-Vidal says, "we can then try and teach stroke victims to think in certain ways and match their own EEG signals with the normal signals." This could "retrain" healthy areas of the brain in what is known as neuroplasticity.

One potential method for retraining comes from one of the Maryland research team's newest members, Steve Graff, a first-year bioengineering doctoral student. He envisions a virtual reality game that matches real EEG data with on-screen characters. "It gives us a way to train someone to think the right thoughts to generate movement from digital avatars. If they can do that, then they can generate thoughts to move a device," says Graff, who brings a unique personal perspective to the work. He has congenital muscular dystrophy and uses a motorized wheelchair. The advances he's working on could allow him to use both hands -- to put on a jacket, dial his cell phone or throw a football while operating his chair with his mind.

No Surgery Required

During the past two decades a great deal of progress has been made in the study of direct brain to computer interfaces, most of it through studies using monkeys with electrodes implanted in their brains. However, for use in humans such an invasive approach poses many problems, not the least of which is that most people don't' want holes in their heads and wires attached to their brains. "EEG monitoring of the brain, which has a long, safe history for other applications, has been largely ignored by those working on brain-machine interfaces, because it was thought that the human skull blocked too much of the detailed information on brain activity needed to read thoughts about movement and turn those readings into movement commands for multi-functional high-degree of freedom prosthetics," said Contreras-Vidal. He is among the few who have used EEG, MEG or other sensing technologies to develop non-invasive neural interfaces, and the only one to have demonstrated decoding results comparable to those achieved by researchers using implanted electrodes.

A paper Contreras-Vidal and colleagues published in the Journal of Neuroscience in March 2010 showed the feasibility of Maryland's EEG-based technology to infer multidimensional natural movement from noninvasive measurements of brain activity. In their two latest studies, Contreras-Vidal and his team have further advanced the development of their EEG brain interface technology, and provided powerful new evidence that it can yield brain computer interface results as good as or better than those from invasive studies, while also requiring minimal training to use.

In a paper published in April in the Journal of Neural Engineering, the Maryland team demonstrated that people wearing the EEG brain cap, could after minimal training control a computer cursor with their thoughts and achieve performance levels comparable to those by subjects using invasive implanted electrode brain computer interface systems. Contreras-Vidal and his co-authors write that this study also shows that compared to studies of other noninvasive brain control interface systems, training time with their system was substantially shorter, requiring only a single 40-minute session.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Maryland.

Journal Reference:

A. Presacco, R. Goodman, L. W. Forrester, J. L. Contreras-Vidal. Neural decoding of treadmill walking from non-invasive, electroencephalographic (EEG) signals. Journal of Neurophysiology, 2011; DOI: 10.1152/jn.00104.2011

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here