A network of chemists at the University of Konstanz has developed an innovative method to study protein structures by means of magnetic labels. The ingenious thing about it is that the magnetic labels are directly incorporated inside the cell when the protein is naturally biosynthesized. The research results, that might have an impact on many areas of structural biology, have been published in the current issue of the renowned scientific journal Journal of the American Chemical Society.
"Unnatural amino acids with special chemical or biophysical functions that are directly incorporated into proteins in the cell have been known for years. However, despite all efforts it has been impossible so far to develop a magnetic unnatural amino acid. Now we have achieved a real breakthrough", says the Konstanz-based chemist Dr. Daniel Summerer about the research project, which has been conducted in collaboration with the working group of the physical chemist Dr. Malte Drescher from Konstanz. "This has brought us a significant step closer to the final objective of measuring the structure and dynamics of proteins directly in the cell with high precision", Summerer explains.
https://plus.google.com/u/0/b/102913432323563044867/102913432323563044867/posts
Proteins that have been modified with the unnatural amino acids from Konstanz can be measured by means of electron paramagnetic resonance spectroscopy (EPR-spectroscopy). Interacting magnetic labels are introduced into strategically selected protein sites. "Measuring the strength of the magnetic interaction enables us to deduce the distance", explains Malte Drescher. "The structure of the protein can be determined by measuring several distances on the nanometer-scale", Drescher reveals the key principle.
In further steps the scientists intend to implement their method, for which they have filed a patent, for the study of protein structures in cells: "Our vision is that we will use our method to investigate biologically relevant systems that play a role in e.g. the Parkinson's disease or in regulating the expression of disease-relevant genes", Malte Drescher provides an outlook for the continuation of the research works.
The research was carried out in close collaboration with the Konstanz Research School Chemical Biology. "I am particularly pleased that with this success the valuable work of our two doctoral students, Moritz Schmidt and Julia Borbas, is recognized", says Summerer. For Moritz Schmidt, who has begun his doctoral programme as a Hoechst scholarship holder of the Aventis Foundation less than two years ago, this study is already the second publication as lead author in a particularly prestigious chemical journal.
Wednesday, January 29, 2014
Caffeine: how does it really affect our health?
When we wake up in the morning, many of us reach for a coffee to kick-start our day. According to the International Coffee Organization, approximately 1.6 billion cups of coffee are consumed worldwide every day.
The US Food and Drug Administration (FDA) state that the average amount of caffeine consumed in the US is approximately 300 mg per person per day - the equivalent to between two and four cups of coffee. This is considered to be a moderate caffeine intake, which according to many studies, can promote a variety of health benefits. http://www.mediafire.com/view/5sp3e211e6b1dxl/Truth
But some studies claim otherwise, even suggesting that one or two cups of coffee a day may negatively impact our health. So, what are we to believe?
We analyze the potential health benefits, as well as the negative side effects of caffeine consumption.
A natural stimulant
The main ingredient in coffee is caffeine - a compound that naturally derives from over 60 different plant sources, including coffee beans, tea leaves, cacao seeds and cola nut seeds.
Caffeine acts as a stimulant by activating the central nervous system. It can combat tiredness and improve concentration and focus.
According to the University of Michigan Health Service, the stimulating effects of caffeine can start as early as 15 minutes after consumption and last up to 6 hours.
Other than coffee, caffeine is commonly consumed through tea, soft drinks - particularly energy drinks - and chocolate. It is also found in some prescription and non-prescription drugs, such as cold, allergy and pain medication.
The potential health benefits
As well as its stimulating effects, caffeine has been heralded for providing an array of health benefits.
A cup of coffee surrounded by coffee beans
Some studies have suggested that drinking three or four cups of coffee a day may reduce the risk of liver, mouth and throat cancer.
Last year, Medical News Today reported on a study suggesting that consuming three cups of coffee a day may reduce the risk of liver cancer by 50%, while another study suggests that drinking four cups a day could halve the risk of mouth and throat cancer.
Caffeine consumption has also been associated with positive effects on the brain.
Last year, a study from the Harvard School of Public Health suggested that drinking between two and four cups of coffee a day may reduce suicide risk in adults, while more recent research found that ingesting 200 mg of caffeine each day may boost long-term memory.
Other studies have also suggested that caffeine intake may protect against type 2 diabetes, Parkinson's disease, cardiovascular disease and stroke.
Caffeine: the 'socially acceptable psychoactive drug'
With so much research claiming that caffeine consumption can benefit our health, and considering the number of products that contain the stimulant, it is no wonder caffeine consumption is so widespread.
But Steven E. Meredith, postdoctoral research fellow at The Johns Hopkins University School of Medicine, told Medical News Today that, perhaps due to widespread consumption, many of us forget that caffeine is a psychoactive substance - a drug that crosses the blood-brain barrier to stimulate the central nervous system.
He said:
"Unlike most other psychoactive substances, caffeine use is socially acceptable, and the drug is widely used. In fact, caffeine is the most commonly used psychoactive substance in the world.
Moreover, the vast majority of caffeine consumers use the substance regularly without apparent harm. These factors likely contribute to the perspective that caffeine is a benign substance that everyone can use without suffering any negative consequences."
The negative effects of caffeine consumption
But of course, there can be negative consequences from caffeine consumption, particularly if ingested in high doses.
The Mayo Clinic state that consuming more than 500-600 mg of caffeine a day may lead to insomnia, nervousness, restlessness, irritability, an upset stomach, a fast heartbeat and even muscle tremors.
However, previous research has linked even moderate amounts of caffeine to negative health effects.
Last year, Medical News Today reported on a study suggesting that consuming 300 mg of caffeine a day during pregnancy may increase the risk of low birth weight babies, while other research suggests that drinking four cups of coffee a day may increase the risk of early death.
Effects of caffeine vary from person to person
But Meredith told us that the effects of caffeine can vary in each individual, which may explain why there are mixed messages surrounding whether caffeine is good or bad for us.
For example, he said that individuals with anxiety disorders are more susceptible to the anxiogenic effects of the compound.
Silhouette of person smoking a cigarette and holding a cup of coffee.
Cigarette smokers can metabolize caffeine twice as fast as non-smokers.
"Caffeine can also metabolize at different rates among individuals for various reasons. For example, cigarette smokers metabolize caffeine twice as fast as non-smokers," he added.
The US Food and Drug Administration (FDA) state that the average amount of caffeine consumed in the US is approximately 300 mg per person per day - the equivalent to between two and four cups of coffee. This is considered to be a moderate caffeine intake, which according to many studies, can promote a variety of health benefits. http://www.mediafire.com/view/5sp3e211e6b1dxl/Truth
But some studies claim otherwise, even suggesting that one or two cups of coffee a day may negatively impact our health. So, what are we to believe?
We analyze the potential health benefits, as well as the negative side effects of caffeine consumption.
A natural stimulant
The main ingredient in coffee is caffeine - a compound that naturally derives from over 60 different plant sources, including coffee beans, tea leaves, cacao seeds and cola nut seeds.
Caffeine acts as a stimulant by activating the central nervous system. It can combat tiredness and improve concentration and focus.
According to the University of Michigan Health Service, the stimulating effects of caffeine can start as early as 15 minutes after consumption and last up to 6 hours.
Other than coffee, caffeine is commonly consumed through tea, soft drinks - particularly energy drinks - and chocolate. It is also found in some prescription and non-prescription drugs, such as cold, allergy and pain medication.
The potential health benefits
As well as its stimulating effects, caffeine has been heralded for providing an array of health benefits.
A cup of coffee surrounded by coffee beans
Some studies have suggested that drinking three or four cups of coffee a day may reduce the risk of liver, mouth and throat cancer.
Last year, Medical News Today reported on a study suggesting that consuming three cups of coffee a day may reduce the risk of liver cancer by 50%, while another study suggests that drinking four cups a day could halve the risk of mouth and throat cancer.
Caffeine consumption has also been associated with positive effects on the brain.
Last year, a study from the Harvard School of Public Health suggested that drinking between two and four cups of coffee a day may reduce suicide risk in adults, while more recent research found that ingesting 200 mg of caffeine each day may boost long-term memory.
Other studies have also suggested that caffeine intake may protect against type 2 diabetes, Parkinson's disease, cardiovascular disease and stroke.
Caffeine: the 'socially acceptable psychoactive drug'
With so much research claiming that caffeine consumption can benefit our health, and considering the number of products that contain the stimulant, it is no wonder caffeine consumption is so widespread.
But Steven E. Meredith, postdoctoral research fellow at The Johns Hopkins University School of Medicine, told Medical News Today that, perhaps due to widespread consumption, many of us forget that caffeine is a psychoactive substance - a drug that crosses the blood-brain barrier to stimulate the central nervous system.
He said:
"Unlike most other psychoactive substances, caffeine use is socially acceptable, and the drug is widely used. In fact, caffeine is the most commonly used psychoactive substance in the world.
Moreover, the vast majority of caffeine consumers use the substance regularly without apparent harm. These factors likely contribute to the perspective that caffeine is a benign substance that everyone can use without suffering any negative consequences."
The negative effects of caffeine consumption
But of course, there can be negative consequences from caffeine consumption, particularly if ingested in high doses.
The Mayo Clinic state that consuming more than 500-600 mg of caffeine a day may lead to insomnia, nervousness, restlessness, irritability, an upset stomach, a fast heartbeat and even muscle tremors.
However, previous research has linked even moderate amounts of caffeine to negative health effects.
Last year, Medical News Today reported on a study suggesting that consuming 300 mg of caffeine a day during pregnancy may increase the risk of low birth weight babies, while other research suggests that drinking four cups of coffee a day may increase the risk of early death.
Effects of caffeine vary from person to person
But Meredith told us that the effects of caffeine can vary in each individual, which may explain why there are mixed messages surrounding whether caffeine is good or bad for us.
For example, he said that individuals with anxiety disorders are more susceptible to the anxiogenic effects of the compound.
Silhouette of person smoking a cigarette and holding a cup of coffee.
Cigarette smokers can metabolize caffeine twice as fast as non-smokers.
"Caffeine can also metabolize at different rates among individuals for various reasons. For example, cigarette smokers metabolize caffeine twice as fast as non-smokers," he added.
Eye movement speed linked to impulsive decision making
One of the most frustrating things about shopping in a grocery store can be the long lines at the cash register. Do you stand there and wait for the line to go down? Or do you join another line that looks quicker? According to new research, decisions such as this may be dependent on the speed of our eye movements.
In a study published in The Journal of Neuroscience, researchers from Johns Hopkins University in Maryland found that people who are less patient are more likely to have faster eye movements.
The investigators say their findings may provide insight into why abnormalities in certain areas of the brain make decision making more challenging for people who have suffered brain injuries or who have neurological disorders, such as schizophrenia.https://plus.google.com/u/0/b/102913432323563044867/102913432323563044867/posts
According to the investigators, previous research from the team suggested that how a person moves may be an indicator of how the brain works out the time frame in which to reduce the value of a reward. For example, when a person determines how long they should stand in line to get their groceries.
For this study, the researchers wanted to see whether differences in eye movements, in place of other body movements, could reflect differences in how a person assesses time and reward.
Saccade speed 'varies from person to person'
The research team monitored eye movements, known as saccades, of healthy volunteers.
close-up view of an eye
Researchers say the speed of our eye movements may determine our level of patience.
Reza Shadmehr, professor of biomedical engineering and neuroscience at Johns Hopkins University and lead researcher, explains that saccades are the motions the eye makes when we switch focus between objects.
He notes that saccades are the fastest movements in the body, occurring in milliseconds. Saccades are at their fastest during teenage years, but they slow down as a person ages.
The volunteers were asked to look at a screen, where a series of dots appeared one at a time. They first appeared on one side of the screen, then the other, before flicking back and forth to each side.
Using a camera to record the participants' saccades, the investigators found that over all participants, saccade speed varied significantly. However, in each individual participant, saccade speed appeared to be consistent - leading the team to believe that the speed of eye movement varies from person to person.
Testing the participants' patience
The research team then conducted another experiment to determine whether saccade speed is associated with impulsivity and decision making.
This also involved the volunteers viewing the screen with the dots. For this experiment, they were instructed to look left or right. A buzzer sounded if they failed a command.
Once the participants were used to this part of the experiment, they were told that if they followed the first commands in the next testing round, they would be incorrect 25% of the time.
They were also told that in the instances they were wrong, after an undisclosed amount of time, the first command would be taken over by a second command to look in the opposite direction.
The investigators changed the length of time between these two commands in order to identify the length of time participants would be willing to wait to improve their test accuracy.
In a study published in The Journal of Neuroscience, researchers from Johns Hopkins University in Maryland found that people who are less patient are more likely to have faster eye movements.
The investigators say their findings may provide insight into why abnormalities in certain areas of the brain make decision making more challenging for people who have suffered brain injuries or who have neurological disorders, such as schizophrenia.https://plus.google.com/u/0/b/102913432323563044867/102913432323563044867/posts
According to the investigators, previous research from the team suggested that how a person moves may be an indicator of how the brain works out the time frame in which to reduce the value of a reward. For example, when a person determines how long they should stand in line to get their groceries.
For this study, the researchers wanted to see whether differences in eye movements, in place of other body movements, could reflect differences in how a person assesses time and reward.
Saccade speed 'varies from person to person'
The research team monitored eye movements, known as saccades, of healthy volunteers.
close-up view of an eye
Researchers say the speed of our eye movements may determine our level of patience.
Reza Shadmehr, professor of biomedical engineering and neuroscience at Johns Hopkins University and lead researcher, explains that saccades are the motions the eye makes when we switch focus between objects.
He notes that saccades are the fastest movements in the body, occurring in milliseconds. Saccades are at their fastest during teenage years, but they slow down as a person ages.
The volunteers were asked to look at a screen, where a series of dots appeared one at a time. They first appeared on one side of the screen, then the other, before flicking back and forth to each side.
Using a camera to record the participants' saccades, the investigators found that over all participants, saccade speed varied significantly. However, in each individual participant, saccade speed appeared to be consistent - leading the team to believe that the speed of eye movement varies from person to person.
Testing the participants' patience
The research team then conducted another experiment to determine whether saccade speed is associated with impulsivity and decision making.
This also involved the volunteers viewing the screen with the dots. For this experiment, they were instructed to look left or right. A buzzer sounded if they failed a command.
Once the participants were used to this part of the experiment, they were told that if they followed the first commands in the next testing round, they would be incorrect 25% of the time.
They were also told that in the instances they were wrong, after an undisclosed amount of time, the first command would be taken over by a second command to look in the opposite direction.
The investigators changed the length of time between these two commands in order to identify the length of time participants would be willing to wait to improve their test accuracy.
Vitamin D deficiency in pregnancy 'increases preeclampsia risk'
Research led by investigators from the University of Pittsburgh Graduate School of Public Health suggests that women who have a vitamin D deficiency in the first 26 weeks of pregnancy are more likely to develop severe preeclampsia. This is according to a study recently published in the journal Epidemiology.
Preeclampsia is a potentially life-threatening pregnancy complication that usually occurs after the first 20 weeks of gestation or shortly after birth. According to the Preeclampsia Foundation, around 5-8% of pregnancies are affected by the condition.
Early signs of the condition include high blood pressure and albuminuria - excess protein that leaks into the urine.https://plus.google.com/u/0/b/102913432323563044867/102913432323563044867/posts
Some women may also experience swelling of the feet, ankles, face and hands - caused by fluid retention - as well as severe headaches, problems with vision and pain just below the ribs.
Vitamin D and pregnancy
Vitamin D is known to be important for regulating and absorbing calcium and phosphorus in the body.
The majority of people are able to get all the vitamin D they need from the sun and various foods, such as oily fish, eggs and fortified fat spreads.
However, according to the Vitamin D Council, pregnancy is a known risk factor for vitamin D deficiency.
Previous research has suggested that vitamin D deficiency during pregnancy may lead to gestational diabetes, increased risk of infections and cesarean section, and low offspring birth weight.
To determine whether there is an association between vitamin D deficiency during pregnancy and risk of preeclampsia, the research team analyzed the blood samples of 700 pregnant women who later developed preeclampsia, alongside the blood samples of 3,000 pregnant women who did not develop the condition.
All samples were collected between 1959 and 1965 from 12 US institutions. The researchers note that the blood samples were well-preserved and they were able to test the samples for vitamin D levels decades after they were collected.
Vitamin D deficiency linked to 40% increased preeclampsia risk
The analysis revealed that women who had insufficient levels of vitamin D during the first 26 weeks of pregnancy were 40% more likely to develop severe preeclampsia, compared with women who had adequate levels of the vitamin in the first 26 weeks' gestation.
However, the researchers did not find any association between vitamin D and mild preeclampsia.
These results were apparent after taking other factors into consideration that could impact a woman's vitamin D levels, such as pre-pregnancy body mass index (BMI), race, smoking, diet, the number of previous pregnancies, physical activity and sunlight exposure.
Commenting on the findings, senior study author Dr. Mark A. Klebanoff, of the Center for Perinatal Research at The Research Institute at Nationwide Children's Hospital and the Department of Pediatrics at The Ohio State University College of Medicine, says:
"Scientists believe that severe preeclampsia and mild preeclampsia have different root causes.
Severe preeclampsia poses much higher health risks to the mother and child, so linking it with a factor that we can easily treat, like vitamin D deficiency, holds great potential."
Dr. Lisa Bodner, of the Department of Epidemiology at the University of Pittsburgh Graduate School of Public Health and lead author of the study, says that if similar results are found in a modern sample of pregnant women, then the role of vitamin D in reducing preeclampsia should be explored further.
"Until then," she adds, "women shouldn't automatically take vitamin D supplements during pregnancy as a result of these findings."
Preeclampsia is a potentially life-threatening pregnancy complication that usually occurs after the first 20 weeks of gestation or shortly after birth. According to the Preeclampsia Foundation, around 5-8% of pregnancies are affected by the condition.
Early signs of the condition include high blood pressure and albuminuria - excess protein that leaks into the urine.https://plus.google.com/u/0/b/102913432323563044867/102913432323563044867/posts
Some women may also experience swelling of the feet, ankles, face and hands - caused by fluid retention - as well as severe headaches, problems with vision and pain just below the ribs.
Vitamin D and pregnancy
Vitamin D is known to be important for regulating and absorbing calcium and phosphorus in the body.
The majority of people are able to get all the vitamin D they need from the sun and various foods, such as oily fish, eggs and fortified fat spreads.
However, according to the Vitamin D Council, pregnancy is a known risk factor for vitamin D deficiency.
Previous research has suggested that vitamin D deficiency during pregnancy may lead to gestational diabetes, increased risk of infections and cesarean section, and low offspring birth weight.
To determine whether there is an association between vitamin D deficiency during pregnancy and risk of preeclampsia, the research team analyzed the blood samples of 700 pregnant women who later developed preeclampsia, alongside the blood samples of 3,000 pregnant women who did not develop the condition.
All samples were collected between 1959 and 1965 from 12 US institutions. The researchers note that the blood samples were well-preserved and they were able to test the samples for vitamin D levels decades after they were collected.
Vitamin D deficiency linked to 40% increased preeclampsia risk
The analysis revealed that women who had insufficient levels of vitamin D during the first 26 weeks of pregnancy were 40% more likely to develop severe preeclampsia, compared with women who had adequate levels of the vitamin in the first 26 weeks' gestation.
However, the researchers did not find any association between vitamin D and mild preeclampsia.
These results were apparent after taking other factors into consideration that could impact a woman's vitamin D levels, such as pre-pregnancy body mass index (BMI), race, smoking, diet, the number of previous pregnancies, physical activity and sunlight exposure.
Commenting on the findings, senior study author Dr. Mark A. Klebanoff, of the Center for Perinatal Research at The Research Institute at Nationwide Children's Hospital and the Department of Pediatrics at The Ohio State University College of Medicine, says:
"Scientists believe that severe preeclampsia and mild preeclampsia have different root causes.
Severe preeclampsia poses much higher health risks to the mother and child, so linking it with a factor that we can easily treat, like vitamin D deficiency, holds great potential."
Dr. Lisa Bodner, of the Department of Epidemiology at the University of Pittsburgh Graduate School of Public Health and lead author of the study, says that if similar results are found in a modern sample of pregnant women, then the role of vitamin D in reducing preeclampsia should be explored further.
"Until then," she adds, "women shouldn't automatically take vitamin D supplements during pregnancy as a result of these findings."
Scientists find neuron that controls how much we eat
By activating a neuron in the prefrontal cortex of a mouse's brain, scientists are able to make the mouse eat more. But what could this mean for humans?
The influence that different areas of the brain may have over eating behaviors is a contentious debate in neurobiology.
"Researchers tend to be either in a camp that believes the control of eating is all regulated from the top down, or from the bottom up," says Ralph DiLeone, senior author of the paper, referring to whether it is "higher" decision-making areas of the brain or more "primitive" brain functions that regulate eating behaviors.
"Both are important and this paper brings a little more neurobiological clarity to the question," DiLeone claims.https://app.box.com/s/qm8ewbt0o855yr59scha
In 2012, Medical News Today reported on a study suggesting that fructose increases activity in the hypothalamus, insula and striatum - areas of the brain responsible for processing motivation and reward. Fructose prevented certain brain cells that instruct us to eat from telling us we are full, and so seemed to increase "food-seeking behavior."
Another 2012 study suggested that a brain receptor called Gpr17 has a role in controlling appetite, and that this could form the basis of potential new anti-obesity medications.
The new study, published in the journal Nature Neuroscience, focuses on the prefrontal cortex - a decision-making area of the brain, which some scientists had suspected may play a role in the eating behaviors of mammals.
Scientists have so far been unable to account for how this relationship between the prefrontal cortex and appetite regulation might work, though.
Switching off neurons prompted mice to eat less
Dopamine, the neurotransmitter that controls the reward and pleasure centers of the brain, is also known to have an important function in food intake.
an overweight mouse eating a leaf
Activating the D1 dopamine-receptor neurons caused the mice to eat more.
Dopamine allows our brain to perceive rewards and to take steps to move toward them. When animals have low levels of dopamine in their brain, they stop eating and eventually die from starvation.
The researchers activated the D1 dopamine-receptor neurons in the prefrontal cortex of mice. They found that this caused the mice to eat more, while inhibiting - or "switching off" - the same neurons caused the mice to eat less.
The dopamine pathway toggled on and off by the scientists in this study also intersects with areas of the brain, such as the amygdala, which process emotional responses.
The researchers think that this could mean eating behavior is regulated at the junction between the decision-making and more primitive emotion centers of the brain.
The authors think that this region of brain circuitry could provide the key to new medication for regulating eating behavior:
The influence that different areas of the brain may have over eating behaviors is a contentious debate in neurobiology.
"Researchers tend to be either in a camp that believes the control of eating is all regulated from the top down, or from the bottom up," says Ralph DiLeone, senior author of the paper, referring to whether it is "higher" decision-making areas of the brain or more "primitive" brain functions that regulate eating behaviors.
"Both are important and this paper brings a little more neurobiological clarity to the question," DiLeone claims.https://app.box.com/s/qm8ewbt0o855yr59scha
In 2012, Medical News Today reported on a study suggesting that fructose increases activity in the hypothalamus, insula and striatum - areas of the brain responsible for processing motivation and reward. Fructose prevented certain brain cells that instruct us to eat from telling us we are full, and so seemed to increase "food-seeking behavior."
Another 2012 study suggested that a brain receptor called Gpr17 has a role in controlling appetite, and that this could form the basis of potential new anti-obesity medications.
The new study, published in the journal Nature Neuroscience, focuses on the prefrontal cortex - a decision-making area of the brain, which some scientists had suspected may play a role in the eating behaviors of mammals.
Scientists have so far been unable to account for how this relationship between the prefrontal cortex and appetite regulation might work, though.
Switching off neurons prompted mice to eat less
Dopamine, the neurotransmitter that controls the reward and pleasure centers of the brain, is also known to have an important function in food intake.
an overweight mouse eating a leaf
Activating the D1 dopamine-receptor neurons caused the mice to eat more.
Dopamine allows our brain to perceive rewards and to take steps to move toward them. When animals have low levels of dopamine in their brain, they stop eating and eventually die from starvation.
The researchers activated the D1 dopamine-receptor neurons in the prefrontal cortex of mice. They found that this caused the mice to eat more, while inhibiting - or "switching off" - the same neurons caused the mice to eat less.
The dopamine pathway toggled on and off by the scientists in this study also intersects with areas of the brain, such as the amygdala, which process emotional responses.
The researchers think that this could mean eating behavior is regulated at the junction between the decision-making and more primitive emotion centers of the brain.
The authors think that this region of brain circuitry could provide the key to new medication for regulating eating behavior:
Stimulating spinal cord protects against Parkinson's symptoms
Long-term treatment that involves electrically stimulating the spinal cord has improved symptoms of Parkinson's disease in rats. Publishing the results of their study in the journal Scientific Reports, researchers from Duke Medicine are hopeful their findings could help human Parkinson's patients.
The team, led by Dr. Miguel Nicolelis, professor of neurobiology at Duke University, built on their own previous research, which showed that stimulating rats' spinal cords with electrical signals temporarily eased symptoms of the disease. https://plus.google.com/u/0/b/102913432323563044867/102913432323563044867/posts
Parkinson's disease is a progressive neurological condition, which is caused by the loss of neurons that produce dopamine in the brain. It affects movement, control of muscles and balance, and it can also cause stiffness, eye problems and sleep problems, among many other symptoms.
"Finding novel treatments that address both the symptoms and progressive nature of Parkinson's disease is a major priority," says Dr. Nicolelis.
The current treatment for Parkinson's is a drug called L-dopa, and it works by replacing dopamine. However, the researchers say it can cause side effects and, over time, lose its effectiveness.
Another emerging therapy is deep brain stimulation. This works through an implant in the brain, which emits electrical signals. But the downside of this technique is that less than 5% of Parkinson's patients qualify for it because it is so invasive.
"We need options that are safe, affordable, effective and can last a long time," says Dr. Nicolelis. He adds that spinal cord stimulation could be the key.
Treatment could protect against loss, damage of neurons
Back in 2009, the Duke University team developed a device that they attached to the spinal cords of rodents that had depleted levels of dopamine.
Chronic Spinal Cord Electrical Stimulation Protects Against 6-hydroxydopamine Lesions
By electrically stimulating the dorsal columns of rats' spinal cords, the researchers found motor skills improved.
Image credit: Duke University School of Medicine
The researchers showed that by sending electrical stimulation to the dorsal column - a sensory pathway that carries information from the body to the brain - the mice and rats no longer had slow, stiff movements, but rather, they appeared as healthy, active animals.
However, because research on this type of stimulation in animals has focused on short-term effects, the team wanted to look at the long-term effects this kind of treatment might yield in rats with Parkinson's symptoms.
So, for 6 weeks, the team applied electrical stimulation to the spinal cord dorsal columns in rats twice a week for 30 minutes.
During this longer-term study, the team saw a "significant improvement" in symptoms. These included improved motor skills and an about-face in severe weight loss.
Additionally, the stimulation was linked to better neuron survival and higher density of "dopaminergic innervation" in two brain regions controlling movement. The loss of this causes Parkinson's disease in humans, the researchers note.
They say their findings suggest that this electrical stimulation may protect against the loss or damage of neurons.
Other uses for dorsal column stimulation
A similar use of dorsal column stimulation is currently being used to lessen chronic pain syndromes in humans, says the team.
They find hope in other small-scale studies in humans that have shown how dorsal column stimulation may also help restore motor function in Parkinson's patients.
However, there is more work to be done, Dr. Nicolelis says:
"This is still a limited number of cases, so studies like ours are important in examining the basic science behind the treatment and the potential mechanisms of why it is effective."
The team, led by Dr. Miguel Nicolelis, professor of neurobiology at Duke University, built on their own previous research, which showed that stimulating rats' spinal cords with electrical signals temporarily eased symptoms of the disease. https://plus.google.com/u/0/b/102913432323563044867/102913432323563044867/posts
Parkinson's disease is a progressive neurological condition, which is caused by the loss of neurons that produce dopamine in the brain. It affects movement, control of muscles and balance, and it can also cause stiffness, eye problems and sleep problems, among many other symptoms.
"Finding novel treatments that address both the symptoms and progressive nature of Parkinson's disease is a major priority," says Dr. Nicolelis.
The current treatment for Parkinson's is a drug called L-dopa, and it works by replacing dopamine. However, the researchers say it can cause side effects and, over time, lose its effectiveness.
Another emerging therapy is deep brain stimulation. This works through an implant in the brain, which emits electrical signals. But the downside of this technique is that less than 5% of Parkinson's patients qualify for it because it is so invasive.
"We need options that are safe, affordable, effective and can last a long time," says Dr. Nicolelis. He adds that spinal cord stimulation could be the key.
Treatment could protect against loss, damage of neurons
Back in 2009, the Duke University team developed a device that they attached to the spinal cords of rodents that had depleted levels of dopamine.
Chronic Spinal Cord Electrical Stimulation Protects Against 6-hydroxydopamine Lesions
By electrically stimulating the dorsal columns of rats' spinal cords, the researchers found motor skills improved.
Image credit: Duke University School of Medicine
The researchers showed that by sending electrical stimulation to the dorsal column - a sensory pathway that carries information from the body to the brain - the mice and rats no longer had slow, stiff movements, but rather, they appeared as healthy, active animals.
However, because research on this type of stimulation in animals has focused on short-term effects, the team wanted to look at the long-term effects this kind of treatment might yield in rats with Parkinson's symptoms.
So, for 6 weeks, the team applied electrical stimulation to the spinal cord dorsal columns in rats twice a week for 30 minutes.
During this longer-term study, the team saw a "significant improvement" in symptoms. These included improved motor skills and an about-face in severe weight loss.
Additionally, the stimulation was linked to better neuron survival and higher density of "dopaminergic innervation" in two brain regions controlling movement. The loss of this causes Parkinson's disease in humans, the researchers note.
They say their findings suggest that this electrical stimulation may protect against the loss or damage of neurons.
Other uses for dorsal column stimulation
A similar use of dorsal column stimulation is currently being used to lessen chronic pain syndromes in humans, says the team.
They find hope in other small-scale studies in humans that have shown how dorsal column stimulation may also help restore motor function in Parkinson's patients.
However, there is more work to be done, Dr. Nicolelis says:
"This is still a limited number of cases, so studies like ours are important in examining the basic science behind the treatment and the potential mechanisms of why it is effective."
Greater experience causes older brains to slow down, study shows
We are all familiar with the saying "older but wiser." And new research may prove this to be true. A new study published in the journal Topics in Cognitive Science suggests that as we age, our brain functions slow down as a result of greater experience, not because of cognitive decline.
According to the research team, led by Dr. Michael Ramscar of the University of Tuebingen in Germany, the reason why brains of older adults slow down is because they take longer to process constantly increasing amounts of knowledge. https://app.box.com/s/qm8ewbt0o855yr59scha
They argue that this process is frequently confused with cognitive decline.
To reach their findings, the investigators programmed computers to act like humans.
Each day, the computers "read" a certain amount of data while processing new information.
The computers then carried out a series of tests using measures that are traditionally used to determine cognitive abilities. These included word recall tests.
Increased knowledge, not cognitive decline
The researchers found that when they limited the computers to reading a set amount, the cognitive performance of the computers was similar to the cognitive performance expected from a young adult.
However, the investigators discovered that when the same computers read unlimited data - the equivalent to a lifetime of experiences - their cognitive performance resembled that of an older adult.
The researchers say that the cognitive performance of the computers slowed down, not because of a decline in processing capacity, but because the unlimited data increased their database, meaning they needed more time to process the information.
Explaining what their findings mean, the study authors write:
"The results reported here indicate that in older and younger adults, performance in psychometric testing are the product of the same cognitive mechanisms processing different quantities of information. Older adults' performance reflects increased knowledge, not cognitive decline."
'False assumptions' about the aging mind
The investigators say that their findings suggest that society needs to rethink what is meant by the "aging mind," as "false assumptions" may deprecate the aging population and lead to wastage of public resources on problems that do not exist.
According to the research team, led by Dr. Michael Ramscar of the University of Tuebingen in Germany, the reason why brains of older adults slow down is because they take longer to process constantly increasing amounts of knowledge. https://app.box.com/s/qm8ewbt0o855yr59scha
They argue that this process is frequently confused with cognitive decline.
To reach their findings, the investigators programmed computers to act like humans.
Each day, the computers "read" a certain amount of data while processing new information.
The computers then carried out a series of tests using measures that are traditionally used to determine cognitive abilities. These included word recall tests.
Increased knowledge, not cognitive decline
The researchers found that when they limited the computers to reading a set amount, the cognitive performance of the computers was similar to the cognitive performance expected from a young adult.
However, the investigators discovered that when the same computers read unlimited data - the equivalent to a lifetime of experiences - their cognitive performance resembled that of an older adult.
The researchers say that the cognitive performance of the computers slowed down, not because of a decline in processing capacity, but because the unlimited data increased their database, meaning they needed more time to process the information.
Explaining what their findings mean, the study authors write:
"The results reported here indicate that in older and younger adults, performance in psychometric testing are the product of the same cognitive mechanisms processing different quantities of information. Older adults' performance reflects increased knowledge, not cognitive decline."
'False assumptions' about the aging mind
The investigators say that their findings suggest that society needs to rethink what is meant by the "aging mind," as "false assumptions" may deprecate the aging population and lead to wastage of public resources on problems that do not exist.
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