Neuroscience

Articles and news from the latest research reports.

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Scientists Find Way to Image Brain Waste Removal Process Which May Lead to Alzheimer’s Diagnostic
A novel way to image the entire brain’s glymphatic pathway, a dynamic process that clears waste and solutes from the brain that otherwise might build-up and contribute to the development of Alzheimer’s disease, may provide the basis for a new strategy to evaluate disease susceptibility, according to a research paper published online in The Journal of Clinical Investigation. Through contrast enhanced magnetic resonance imaging (MRI) and other tools, a Stony Brook University-led research team successfully mapped this brain-wide pathway and identified key anatomical clearance routes of brain waste.
In their article titled “Brain-wide pathway for waste clearance captured by contrast enhanced MRI,” Principal Investigator Helene Benveniste, MD, PhD, a Professor in the Departments of Anesthesiology and Radiology at Stony Brook University School of Medicine, and colleagues built upon a previous finding by Jeffrey Iliff, PhD, and Maiken Nedergaard, MD, PhD, from University of Rochester that initially discovered and defined the glymphatic pathway, where cerebral spinal fluid (CSF) filters through the brain and exchanges with interstitial fluid (ISF) to clear waste, similar to the way lymphatic vessels clear waste from other organs of the body. Despite the discovery of the glymphatic pathway, researchers could not visualize the brain wide flow of this pathway with previous imaging techniques.
“Our experiments showed proof of concept that the glymphatic pathway function can be measured using a simple and clinically relevant imaging technique,” said Dr. Benveniste. “This technique provides a three-dimensional view of the glymphatic pathway that captures movement of waste and solutes in real time. This will help us to define the role of the pathway in clearing matter such as amyloid beta and tau proteins, which affect brain processes if they build up.”
Dr. Benveniste said that the pathology of certain neurological conditions is associated with the accumulation of these proteins and other large extracellular aggregates. In particular, she explained that plaque deposits of these proteins are implicated in the development of Alzheimer’s disease, as well as chronic traumatic encephalopathy that occurs after repetitive mild traumatic brain injuries.

Scientists Find Way to Image Brain Waste Removal Process Which May Lead to Alzheimer’s Diagnostic

A novel way to image the entire brain’s glymphatic pathway, a dynamic process that clears waste and solutes from the brain that otherwise might build-up and contribute to the development of Alzheimer’s disease, may provide the basis for a new strategy to evaluate disease susceptibility, according to a research paper published online in The Journal of Clinical Investigation. Through contrast enhanced magnetic resonance imaging (MRI) and other tools, a Stony Brook University-led research team successfully mapped this brain-wide pathway and identified key anatomical clearance routes of brain waste.

In their article titled “Brain-wide pathway for waste clearance captured by contrast enhanced MRI,” Principal Investigator Helene Benveniste, MD, PhD, a Professor in the Departments of Anesthesiology and Radiology at Stony Brook University School of Medicine, and colleagues built upon a previous finding by Jeffrey Iliff, PhD, and Maiken Nedergaard, MD, PhD, from University of Rochester that initially discovered and defined the glymphatic pathway, where cerebral spinal fluid (CSF) filters through the brain and exchanges with interstitial fluid (ISF) to clear waste, similar to the way lymphatic vessels clear waste from other organs of the body. Despite the discovery of the glymphatic pathway, researchers could not visualize the brain wide flow of this pathway with previous imaging techniques.

“Our experiments showed proof of concept that the glymphatic pathway function can be measured using a simple and clinically relevant imaging technique,” said Dr. Benveniste. “This technique provides a three-dimensional view of the glymphatic pathway that captures movement of waste and solutes in real time. This will help us to define the role of the pathway in clearing matter such as amyloid beta and tau proteins, which affect brain processes if they build up.”

Dr. Benveniste said that the pathology of certain neurological conditions is associated with the accumulation of these proteins and other large extracellular aggregates. In particular, she explained that plaque deposits of these proteins are implicated in the development of Alzheimer’s disease, as well as chronic traumatic encephalopathy that occurs after repetitive mild traumatic brain injuries.

Filed under brain glymphatic pathway MRI alzheimer's disease brain waste tau proteins neuroscience science

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Scientists find genes linked to human neurological disorders in sea lamprey genome
Scientists at the Marine Biological Laboratory (MBL) have identified several genes linked to human neurological disorders, including Alzheimer’s disease, Parkinson’s disease and spinal cord injury, in the sea lamprey, a vertebrate fish whose whole-genome sequence is reported this week in the journal Nature Genetics.
"This means that we can use the sea lamprey as a powerful model to drive forward our molecular understanding of human neurodegenerative disease and neurological disorders," says Jennifer Morgan of the MBL’s Eugene Bell Center for Regenerative Biology and Tissue Engineering. The ultimate goals are to determine what goes wrong with neurons after injury and during disease, and to determine how to correct these deficits in order to restore normal nervous system functions.
Unlike humans, the lamprey has an extraordinary capacity to regenerate its nervous system. If a lamprey’s spinal cord is severed, it can regenerate the damaged nerve cells and be swimming again in 10-12 weeks.
Morgan and her collaborators at MBL, Ona Bloom and Joseph Buxbaum, have been studying the lamprey’s recovery from spinal cord injury since 2009. The lamprey has large, identified neurons in its brain and spinal cord, making it an excellent model to study regeneration at the single cell-level. Now, the lamprey’s genomic information gives them a whole new “toolkit” for understanding its regenerative mechanisms, and for comparing aspects of its physiology, such as inflammation response, to that of humans.
The lamprey genome project was accomplished by a consortium of 59 researchers led by Weiming Li of Michigan State University and Jeramiah Smith of the University of Kentucky. The MBL scientists’ contribution focused on neural aspects of the genome, including one of the project’s most intriguing findings.
Lampreys, in contrast to humans, don’t have myelin, an insulating sheath around neurons that allows faster conduction of nerve impulses. Yet the consortium found genes expressed in the lamprey that are normally expressed in myelin. In humans, myelin-associated molecules inhibit nerves from regenerating if damaged. “A lot of the focus of the spinal cord injury field is on neutralizing those inhibitory molecules,” Morgan says.
"So there is an interesting conundrum," Morgan says. "What are these myelin-associated genes doing in an animal that doesn’t have myelin, and yet is good at regeneration? It opens up a new and interesting set of questions, " she says. Addressing them could bring insight to why humans lost the capacity for neural regeneration long ago, and how this might be restored.
At present, Morgan and her collaborators are focused on analyzing which genes are expressed and when, after spinal cord injury and regeneration. The whole-genome sequence gives them an invaluable reference for their work.

Scientists find genes linked to human neurological disorders in sea lamprey genome

Scientists at the Marine Biological Laboratory (MBL) have identified several genes linked to human neurological disorders, including Alzheimer’s disease, Parkinson’s disease and spinal cord injury, in the sea lamprey, a vertebrate fish whose whole-genome sequence is reported this week in the journal Nature Genetics.

"This means that we can use the sea lamprey as a powerful model to drive forward our molecular understanding of human neurodegenerative disease and neurological disorders," says Jennifer Morgan of the MBL’s Eugene Bell Center for Regenerative Biology and Tissue Engineering. The ultimate goals are to determine what goes wrong with neurons after injury and during disease, and to determine how to correct these deficits in order to restore normal nervous system functions.

Unlike humans, the lamprey has an extraordinary capacity to regenerate its nervous system. If a lamprey’s spinal cord is severed, it can regenerate the damaged nerve cells and be swimming again in 10-12 weeks.

Morgan and her collaborators at MBL, Ona Bloom and Joseph Buxbaum, have been studying the lamprey’s recovery from spinal cord injury since 2009. The lamprey has large, identified neurons in its brain and spinal cord, making it an excellent model to study regeneration at the single cell-level. Now, the lamprey’s genomic information gives them a whole new “toolkit” for understanding its regenerative mechanisms, and for comparing aspects of its physiology, such as inflammation response, to that of humans.

The lamprey genome project was accomplished by a consortium of 59 researchers led by Weiming Li of Michigan State University and Jeramiah Smith of the University of Kentucky. The MBL scientists’ contribution focused on neural aspects of the genome, including one of the project’s most intriguing findings.

Lampreys, in contrast to humans, don’t have myelin, an insulating sheath around neurons that allows faster conduction of nerve impulses. Yet the consortium found genes expressed in the lamprey that are normally expressed in myelin. In humans, myelin-associated molecules inhibit nerves from regenerating if damaged. “A lot of the focus of the spinal cord injury field is on neutralizing those inhibitory molecules,” Morgan says.

"So there is an interesting conundrum," Morgan says. "What are these myelin-associated genes doing in an animal that doesn’t have myelin, and yet is good at regeneration? It opens up a new and interesting set of questions, " she says. Addressing them could bring insight to why humans lost the capacity for neural regeneration long ago, and how this might be restored.

At present, Morgan and her collaborators are focused on analyzing which genes are expressed and when, after spinal cord injury and regeneration. The whole-genome sequence gives them an invaluable reference for their work.

Filed under sea lamprey neurodegenerative diseases neurological disorders nervous system spinal cord injury neuroscience science

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Ability of brain to protect itself from damage revealed

image

(Image: Matthias Kulka / Corbis)

The origin of an innate ability the brain has to protect itself from damage that occurs in stroke has been explained for the first time.

The Oxford University researchers hope that harnessing this inbuilt biological mechanism, identified in rats, could help in treating stroke and preventing other neurodegenerative diseases in the future.

'We have shown for the first time that the brain has mechanisms that it can use to protect itself and keep brain cells alive,' says Professor Alastair Buchan, Head of the Medical Sciences Division and Dean of the Medical School at Oxford University, who led the work.

The researchers report their findings in the journal Nature Medicine and were funded by the UK Medical Research Council and National Institute for Health Research.

Stroke is the third most common cause of death in the UK. Every year around 150,000 people in the UK have a stroke.

It occurs when the blood supply to part of the brain is cut off. When this happens, brain cells are deprived of the oxygen and nutrients they need to function properly, and they begin to die.

'Time is brain, and the clock has started immediately after the onset of a stroke. Cells will start to die somewhere from minutes to at most 1 or 2 hours after the stroke,' says Professor Buchan.

This explains why treatment for stroke is so dependent on speed. The faster someone can reach hospital, be scanned and have drugs administered to dissolve any blood clot and get the blood flow re-started, the less damage to brain cells there will be.

It has also motivated a so-far unsuccessful search for ‘neuroprotectants’: drugs that can buy time and help the brain cells, or neurons, cope with damage and recover afterwards.

The Oxford University research group have now identified the first example of the brain having its own built-in form of neuroprotection, so-called ‘endogenous neuroprotection’.

They did this by going back to an observation first made over 85 years ago. It has been known since 1926 that neurons in one area of the hippocampus, the part of the brain that controls memory, are able to survive being starved of oxygen, while others in a different area of the hippocampus die. But what protected that one set of cells from damage had remained a puzzle until now.

'Previous studies have focused on understanding how cells die after being depleted of oxygen and glucose. We considered a more direct approach by investigating the endogenous mechanisms that have evolved to make these cells in the hippocampus resistant,' explains first author Dr Michalis Papadakis, Scientific Director of the Laboratory of Cerebral Ischaemia at Oxford University.

Working in rats, the researchers found that production of a specific protein called hamartin allowed the cells to survive being starved of oxygen and glucose, as would happen after a stroke.

They showed that the neurons die in the other part of the hippocampus because of a lack of the hamartin response.

The team was then able to show that stimulating production of hamartin offered greater protection for the neurons.

Professor Buchan says: ‘This is causally related to cell survival. If we block hamartin, the neurons die when blood flow is stopped. If we put hamartin back, the cells survive once more.’

Finally, the researchers were able to identify the biological pathway through which hamartin acts to enable the nerve cells to cope with damage when starved of energy and oxygen.

The group points out that knowing the natural biological mechanism that leads to neuroprotection opens up the possibility of developing drugs that mimic hamartin’s effect.

Professor Buchan says: ‘There is a great deal of work ahead if this is to be translated into the clinic, but we now have a neuroprotective strategy for the first time. Our next steps will be to see if we can find small molecule drug candidates that mimic what hamartin does and keep brain cells alive.

'While we are focussing on stroke, neuroprotective drugs may also be of interest in other conditions that see early death of brain cells including Alzheimer's and motor neurone disease,' he suggests.

(Source: eurekalert.org)

Filed under neurodegenerative diseases brain brain cells stroke endogenous neuroprotection hippocampus neuroscience science

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How electrodes in the brain block obsessive behaviour
Deep brain stimulation helps some people with obsessive-compulsive disorder (OCD), but no one was quite sure why it is effective. A new study offers an explanation: the stimulation has surprisingly pervasive effects, fixing abnormal signalling between different parts of the brain.
A small number of people with difficult-to-treat OCD have had electrodes permanently implanted deep within their brain. Stimulating these electrodes reduces their symptoms.
To work out why stimulation has this effect, Damiaan Denys and Martijn Figee at the Academic Medical Center in Amsterdam, the Netherlands, and colleagues recorded neural activity in people with electrodes implanted into a part of the brain called the nucleus accumbens. This region is vital for conveying motivational and emotional information to the frontal cortex to guide decisions on what actions to take next. In some people with OCD, feedback loops between the two get jammed, leading them to do the same task repeatedly to reduce anxiety.
The researchers took fMRI scans as participants rested. In 13 people with OCD and implanted electrodes, there was continuous and excessive exchange of signals between the nucleus accumbens and the frontal cortex that was not seen in 11 control subjects. When the electrodes were activated, though, the neural activity of both brain regions in the people with OCD became virtually identical to that in the controls.
The researchers also used EEGs to monitor electrical activity in the brain as the 13 people with OCD viewed images linked with their obsessions, such as cleaning toilets. This time, the team observed excessive activity in the frontal cortex – and again, this activity disappeared when the electrodes were activated.
"The most striking thing is that stimulation doesn’t just affect the nucleus accumbens, but the whole network linked up with the cortex," says Figee.
The study suggests that the electrodes do more than normalise brain activity at the site where they are implanted, as had been assumed. Rather, they appear to repair entire brain circuits that had been faulty. “It resets and normalises these circuits,” says Figee.
Thomas Schlaepfer at the University of Bonn, Germany, points out that such work may allow researchers to use deep brain stimulation to learn about the causes of OCD as they treat it. “It will serve as a research platform informing us about the underlying neurobiology of such disorders,” he says.
(Image courtesy: Michael S. Okun)

How electrodes in the brain block obsessive behaviour

Deep brain stimulation helps some people with obsessive-compulsive disorder (OCD), but no one was quite sure why it is effective. A new study offers an explanation: the stimulation has surprisingly pervasive effects, fixing abnormal signalling between different parts of the brain.

A small number of people with difficult-to-treat OCD have had electrodes permanently implanted deep within their brain. Stimulating these electrodes reduces their symptoms.

To work out why stimulation has this effect, Damiaan Denys and Martijn Figee at the Academic Medical Center in Amsterdam, the Netherlands, and colleagues recorded neural activity in people with electrodes implanted into a part of the brain called the nucleus accumbens. This region is vital for conveying motivational and emotional information to the frontal cortex to guide decisions on what actions to take next. In some people with OCD, feedback loops between the two get jammed, leading them to do the same task repeatedly to reduce anxiety.

The researchers took fMRI scans as participants rested. In 13 people with OCD and implanted electrodes, there was continuous and excessive exchange of signals between the nucleus accumbens and the frontal cortex that was not seen in 11 control subjects. When the electrodes were activated, though, the neural activity of both brain regions in the people with OCD became virtually identical to that in the controls.

The researchers also used EEGs to monitor electrical activity in the brain as the 13 people with OCD viewed images linked with their obsessions, such as cleaning toilets. This time, the team observed excessive activity in the frontal cortex – and again, this activity disappeared when the electrodes were activated.

"The most striking thing is that stimulation doesn’t just affect the nucleus accumbens, but the whole network linked up with the cortex," says Figee.

The study suggests that the electrodes do more than normalise brain activity at the site where they are implanted, as had been assumed. Rather, they appear to repair entire brain circuits that had been faulty. “It resets and normalises these circuits,” says Figee.

Thomas Schlaepfer at the University of Bonn, Germany, points out that such work may allow researchers to use deep brain stimulation to learn about the causes of OCD as they treat it. “It will serve as a research platform informing us about the underlying neurobiology of such disorders,” he says.

(Image courtesy: Michael S. Okun)

Filed under OCD deep brain stimulation brain stimulation compulsive behavior nucleus accumbens neuroscience science

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Insects inspiring new technology
Scientists from the University of Lincoln and Newcastle University have created a computerised system which allows for autonomous navigation of mobile robots based on the locust’s unique visual system.
The work could provide the blueprint for the development of highly accurate vehicle collision sensors, surveillance technology and even aid video game programming according to the research published today.
Locusts have a distinctive way of processing information through electrical and chemical signals, giving them an extremely fast and accurate warning system for impending collisions.
The insect has incredibly powerful data processing systems built into its biology, which can in theory be recreated in robotics.
Inspired by the visual processing power built into these insects’ biology, Professor Shigang Yue from the University of Lincoln’s School of Computer Science and Dr Claire Rind from Newcastle University’s Institute of Neuroscience created the computerised system.
Their findings are published in the International Journal of Advanced Mechatronic Systems.
The research started by understanding the anatomy, responses and development of the circuits in the locust brain that allow it to detect approaching objects and avoid them when in flight or on the ground.
A visually stimulated motor control (VSMC) system was then created which consists of two movement detector types and a simple motor command generator. Each detector processes images and extracts relevant visual clues which are then converted into motor commands.
Prof Yue said: “We were inspired by the way the locusts’ visual system works when interacting with the outside world and the potential to simulate such complex systems in software and hardware for various applications. We created a system inspired by the locusts’ motion sensitive interneuron – the lobula giant movement detector. This system was then used in a robot to enable it to explore paths or interact with objects, effectively using visual input only.”
Funded by the European Union’s Seventh Framework Programme (FP7), the research was carried out as part of a collaborative project with the University of Hamburg in Germany and Tsinghua University and Xi’an Jiaotong University, China.

Insects inspiring new technology

Scientists from the University of Lincoln and Newcastle University have created a computerised system which allows for autonomous navigation of mobile robots based on the locust’s unique visual system.

The work could provide the blueprint for the development of highly accurate vehicle collision sensors, surveillance technology and even aid video game programming according to the research published today.

Locusts have a distinctive way of processing information through electrical and chemical signals, giving them an extremely fast and accurate warning system for impending collisions.

The insect has incredibly powerful data processing systems built into its biology, which can in theory be recreated in robotics.

Inspired by the visual processing power built into these insects’ biology, Professor Shigang Yue from the University of Lincoln’s School of Computer Science and Dr Claire Rind from Newcastle University’s Institute of Neuroscience created the computerised system.

Their findings are published in the International Journal of Advanced Mechatronic Systems.

The research started by understanding the anatomy, responses and development of the circuits in the locust brain that allow it to detect approaching objects and avoid them when in flight or on the ground.

A visually stimulated motor control (VSMC) system was then created which consists of two movement detector types and a simple motor command generator. Each detector processes images and extracts relevant visual clues which are then converted into motor commands.

Prof Yue said: “We were inspired by the way the locusts’ visual system works when interacting with the outside world and the potential to simulate such complex systems in software and hardware for various applications. We created a system inspired by the locusts’ motion sensitive interneuron – the lobula giant movement detector. This system was then used in a robot to enable it to explore paths or interact with objects, effectively using visual input only.”

Funded by the European Union’s Seventh Framework Programme (FP7), the research was carried out as part of a collaborative project with the University of Hamburg in Germany and Tsinghua University and Xi’an Jiaotong University, China.

Filed under robots robotics mobile robots navigation locust visual stimulation neural networks neuroscience science

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Students invited to take cocaine for London university’s research

A London university has offered its students the chance to take part in a clinical trial of cocaine in a bid to understand how the Class A drug affects the body.

King’s College London has sent an email to hundreds of undergraduates inviting them to “take part in a clinical study involving nasal administration of cocaine”.
Students who use drugs recreationally will not be allowed to participate, nor those studying medicine or dentistry. Those who are accepted will be given “reasonable financial compensation” for the time and expenses incurred. The email explains the study will mean that: “After cocaine administration, repeated biological samples (blood, urine, hair, sweat, oral fluid) will be taken to compare and investigate how cocaine and its metabolites are spread through the human body.”
Participants will not be able to cut or dye their hair for 120 days during the study follow-up period as scientists investigate a wide range of physical effects on the body.
The project, which has been approved by London Westminster Research Ethics Committee, will be supervised by the clinical toxicology department at St Thomas’ Hospital.
A spokesman for King’s said: “This is an important scientific study to investigate how cocaine and its metabolites are spread through the human body.
“All the relevant ethical approvals were received for this study. The study will be conducted under the highest level of medical supervision in a dedicated clinical research suite. Further information about the NHS ethical approval process, which was followed, is available on our website.”
The email has already attracted online comments and jokes from students. The university has a reputation for research into the use and effects of illegal drugs, including studies into the genetic causes of addiction and papers on whether certain substances should be legalised.
An estimated 700,000 people in Britain took cocaine last year, making it the second most popular drug after cannabis.

Students invited to take cocaine for London university’s research

A London university has offered its students the chance to take part in a clinical trial of cocaine in a bid to understand how the Class A drug affects the body.

King’s College London has sent an email to hundreds of undergraduates inviting them to “take part in a clinical study involving nasal administration of cocaine”.

Students who use drugs recreationally will not be allowed to participate, nor those studying medicine or dentistry. Those who are accepted will be given “reasonable financial compensation” for the time and expenses incurred. The email explains the study will mean that: “After cocaine administration, repeated biological samples (blood, urine, hair, sweat, oral fluid) will be taken to compare and investigate how cocaine and its metabolites are spread through the human body.”

Participants will not be able to cut or dye their hair for 120 days during the study follow-up period as scientists investigate a wide range of physical effects on the body.

The project, which has been approved by London Westminster Research Ethics Committee, will be supervised by the clinical toxicology department at St Thomas’ Hospital.

A spokesman for King’s said: “This is an important scientific study to investigate how cocaine and its metabolites are spread through the human body.

“All the relevant ethical approvals were received for this study. The study will be conducted under the highest level of medical supervision in a dedicated clinical research suite. Further information about the NHS ethical approval process, which was followed, is available on our website.”

The email has already attracted online comments and jokes from students. The university has a reputation for research into the use and effects of illegal drugs, including studies into the genetic causes of addiction and papers on whether certain substances should be legalised.

An estimated 700,000 people in Britain took cocaine last year, making it the second most popular drug after cannabis.

Filed under cocaine recreational drug use stimulants research medicine science

410 notes

Groundbreaking treatment that enabled paralysed animals to walk again will be tested on humans within months
Scientists behind groundbreaking research that enabled rats with severed spines to run again after two weeks have outlined their plans for human trials.
The technology brings fresh hope to sufferers of spinal cord injuries, and the team say they hope the first humans could be implanted with the technology within months.
Using a cocktail of drugs and electrical impulses, researchers hope to begin testing the project to ‘regrow’ nerves linking the spinal cord to the brain in five patients in a Swiss clinic.
Last June in the journal Science, Grégoire Courtine, of the École Polytechnique Fédérale de Lausanne (EPFL), reported that rats in his lab are not only voluntarily initiating a walking gait, but they were sprinting, climbing up stairs, and avoiding obstacles after a couple of weeks of neurorehabilitation with a combination of a robotic harness and electrical and chemical stimulation.
At the 2013 Annual Meeting of the American Association for the Advancement of Science (AAAS) in Boston, Courtine revealed the next step for the research.
He has since repeated the study in rats with bruised spines, which more closely resembles human trauma patients, and after a few weeks they could walk with no assistance.
He now believes that the technique could help people who have been immobile for up to two years.
Although full human trials are still a few years off, he plans to attempt electrical stimulation on five patients who have limited leg movement in the coming months.
‘We know that spinal cord stimulation is safe, we know that training is good, so we want to start the first trial in people who can move their legs but cannot walk independently.
'So we will implant five patients, we have a new technology which allows us to stimulate the spinal cord of humans just like we do in the rats.’
Once they have refined the technique, they hope to fully rehabilitate patients with moderately damaged spines, while others would regain some movement.
‘We already have preliminary data from the rats with these clinically relevant lesions is that a number of them would recover at the end of the training and could walk without any help. It depends on the severity of the damage,’ he said.
‘But if you talk to the patient and you tell them at least you could use it at home to cook, to watch TV and have normal activity, they say their life would be so different. So it is less ambitious, but we are talking about improving the quality of life, allowing people to stand and take a few steps at home with a walker.’

Groundbreaking treatment that enabled paralysed animals to walk again will be tested on humans within months

Scientists behind groundbreaking research that enabled rats with severed spines to run again after two weeks have outlined their plans for human trials.

The technology brings fresh hope to sufferers of spinal cord injuries, and the team say they hope the first humans could be implanted with the technology within months.

Using a cocktail of drugs and electrical impulses, researchers hope to begin testing the project to ‘regrow’ nerves linking the spinal cord to the brain in five patients in a Swiss clinic.

Last June in the journal Science, Grégoire Courtine, of the École Polytechnique Fédérale de Lausanne (EPFL), reported that rats in his lab are not only voluntarily initiating a walking gait, but they were sprinting, climbing up stairs, and avoiding obstacles after a couple of weeks of neurorehabilitation with a combination of a robotic harness and electrical and chemical stimulation.

At the 2013 Annual Meeting of the American Association for the Advancement of Science (AAAS) in Boston, Courtine revealed the next step for the research.

He has since repeated the study in rats with bruised spines, which more closely resembles human trauma patients, and after a few weeks they could walk with no assistance.

He now believes that the technique could help people who have been immobile for up to two years.

Although full human trials are still a few years off, he plans to attempt electrical stimulation on five patients who have limited leg movement in the coming months.

‘We know that spinal cord stimulation is safe, we know that training is good, so we want to start the first trial in people who can move their legs but cannot walk independently.

'So we will implant five patients, we have a new technology which allows us to stimulate the spinal cord of humans just like we do in the rats.’

Once they have refined the technique, they hope to fully rehabilitate patients with moderately damaged spines, while others would regain some movement.

‘We already have preliminary data from the rats with these clinically relevant lesions is that a number of them would recover at the end of the training and could walk without any help. It depends on the severity of the damage,’ he said.

‘But if you talk to the patient and you tell them at least you could use it at home to cook, to watch TV and have normal activity, they say their life would be so different. So it is less ambitious, but we are talking about improving the quality of life, allowing people to stand and take a few steps at home with a walker.’

Filed under spinal cord stimulation spinal cord injuries electrical stimulation chronic paralysis neuroscience science

46 notes

A how-to manual for fruit fly research has been created
The first ever basic training package to teach students and scientists how to best use the fruit fly, Drosophila, for research has been published. It’s hoped it will encourage more researchers working on a range of conditions from cancer to Alzheimer’s disease to use the humble fly.
The unique scheme has been put together by Dr Andreas Prokop from the Faculty of Life Sciences at the University of Manchester and John Roote from the Department of Genetics at the University of Cambridge.
John Roote said, “In 1910 Thomas Hunt Morgan isolated the first Drosophila sex-linked mutation, white.  Since then many thousands of research workers have realised the potential of the humble fruit fly.
“The powerful research tools that we have today combined with a century of background knowledge, the vast collections of stocks that are available to everyone and the fortuitous ‘pre-adaptation’ of the fly for life in a laboratory ensure that Drosophila melanogaster maintains its position as the pre-eminent model organism for research in genetics.  However, until now a comprehensive teaching programme to guide students through the often daunting first few steps has been surprisingly absent.”
Dr Prokop said: “People don’t realise just how useful the tiny fruit fly can be when it comes to research. Fellow scientists are often not aware of their genetic value for research. For example, about 75% of known human disease genes have a recognisable match in the genome of fruit flies which means they can be used to study the fundamental biology behind complex conditions such as epilepsy or neurodegeneration.”
Fruit flies have been used for scientific research for more than a hundred years. They have allowed scientific breakthroughs in genetics, body structure and function. The first jet lag gene and the first learning gene were identified in flies as well as breakthroughs in neuroscience, such as the discovery of the first channel proteins.
Training package: How to design a genetic mating scheme: a basic training package for Drosophila genetics

A how-to manual for fruit fly research has been created

The first ever basic training package to teach students and scientists how to best use the fruit fly, Drosophila, for research has been published. It’s hoped it will encourage more researchers working on a range of conditions from cancer to Alzheimer’s disease to use the humble fly.

The unique scheme has been put together by Dr Andreas Prokop from the Faculty of Life Sciences at the University of Manchester and John Roote from the Department of Genetics at the University of Cambridge.

John Roote said, “In 1910 Thomas Hunt Morgan isolated the first Drosophila sex-linked mutation, white.  Since then many thousands of research workers have realised the potential of the humble fruit fly.

“The powerful research tools that we have today combined with a century of background knowledge, the vast collections of stocks that are available to everyone and the fortuitous ‘pre-adaptation’ of the fly for life in a laboratory ensure that Drosophila melanogaster maintains its position as the pre-eminent model organism for research in genetics.  However, until now a comprehensive teaching programme to guide students through the often daunting first few steps has been surprisingly absent.”

Dr Prokop said: “People don’t realise just how useful the tiny fruit fly can be when it comes to research. Fellow scientists are often not aware of their genetic value for research. For example, about 75% of known human disease genes have a recognisable match in the genome of fruit flies which means they can be used to study the fundamental biology behind complex conditions such as epilepsy or neurodegeneration.”

Fruit flies have been used for scientific research for more than a hundred years. They have allowed scientific breakthroughs in genetics, body structure and function. The first jet lag gene and the first learning gene were identified in flies as well as breakthroughs in neuroscience, such as the discovery of the first channel proteins.

Training package: How to design a genetic mating scheme: a basic training package for Drosophila genetics

Filed under fruit fly drosophila training package research genetics neurodegeneration neuroscience education science

312 notes

The Amazing Story Of The $300 Glasses That Correct Colorblindness
Mark Changizi and Tim Barber turned research on human vision and blood flow into colorblindness-correcting glasses you can buy on Amazon. Here’s how they did it. 
About 10 years ago, Mark Changizi started to develop research on human vision and how it could see changes in skin color. Like many academics, Changizi, an accomplished neurobiologist, went on to pen a book. The Vision Revolution challenged prevailing theories—no, we don’t see red only to spot berries and fruits amid the vegetation—and detailed the amazing capabilities of why we see the way we do.
If it were up to academia, Changizi’s story might have ended there. “I started out in math and physics, trying to understand the beauty in these fields,” he says, “You are taught, or come to believe, that applying something useful is inherently not interesting.”
Not only did Changizi manage to beat that impulse out of himself, but he and Tim Barber, a friend from middle school, teamed up several years ago to form a joint research institute. 2AI Labs allows the pair to focus on research into cognition and perception in humans and machines, and then to commercialize it. The most recent project? A pair of glasses with filters that just happen to cure colorblindness.
Changizi and Barber didn’t set out to cure colorblindness. Changizi just put forth the idea that humans’ ability to see colors evolved to detect oxygenation and hemoglobin changes in the skin so they could tell if someone was scared, uncomfortable or unhealthy. “We as humans blush and blanche, regardless of overall skin tone,” Barber explains, “We associate color with emotion. People turn purple with anger in every culture.” Once Changizi fully understood the connection between color vision and blood physiology, Changizi determined it would be possible to build filters that aimed to enhance the ability to see those subtle changes by making veins more or less distinct—by sharpening the ability to see the red-green or blue-yellow parts of the spectrum. He and Barber then began the process of patenting their invention.
When they started thinking about commercial applications, Changizi and Barber both admit their minds went straight to television cameras. Changizi was fascinated by the possibilities of infusing an already-enhanced HDTV experience with the capacity to see colors even more clearly.
“We looked into cameras photo receptors and decided that producing a filter for a camera would be too difficult and expensive,” Barber says. The easiest possible approach was not electronic at all, he says. Instead, they worked to develop a lens that adjusts the color signal that hits the human eye and the O2Amp was born.
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The Amazing Story Of The $300 Glasses That Correct Colorblindness

Mark Changizi and Tim Barber turned research on human vision and blood flow into colorblindness-correcting glasses you can buy on Amazon. Here’s how they did it.

About 10 years ago, Mark Changizi started to develop research on human vision and how it could see changes in skin color. Like many academics, Changizi, an accomplished neurobiologist, went on to pen a book. The Vision Revolution challenged prevailing theories—no, we don’t see red only to spot berries and fruits amid the vegetation—and detailed the amazing capabilities of why we see the way we do.

If it were up to academia, Changizi’s story might have ended there. “I started out in math and physics, trying to understand the beauty in these fields,” he says, “You are taught, or come to believe, that applying something useful is inherently not interesting.”

Not only did Changizi manage to beat that impulse out of himself, but he and Tim Barber, a friend from middle school, teamed up several years ago to form a joint research institute. 2AI Labs allows the pair to focus on research into cognition and perception in humans and machines, and then to commercialize it. The most recent project? A pair of glasses with filters that just happen to cure colorblindness.

Changizi and Barber didn’t set out to cure colorblindness. Changizi just put forth the idea that humans’ ability to see colors evolved to detect oxygenation and hemoglobin changes in the skin so they could tell if someone was scared, uncomfortable or unhealthy. “We as humans blush and blanche, regardless of overall skin tone,” Barber explains, “We associate color with emotion. People turn purple with anger in every culture.” Once Changizi fully understood the connection between color vision and blood physiology, Changizi determined it would be possible to build filters that aimed to enhance the ability to see those subtle changes by making veins more or less distinct—by sharpening the ability to see the red-green or blue-yellow parts of the spectrum. He and Barber then began the process of patenting their invention.

When they started thinking about commercial applications, Changizi and Barber both admit their minds went straight to television cameras. Changizi was fascinated by the possibilities of infusing an already-enhanced HDTV experience with the capacity to see colors even more clearly.

“We looked into cameras photo receptors and decided that producing a filter for a camera would be too difficult and expensive,” Barber says. The easiest possible approach was not electronic at all, he says. Instead, they worked to develop a lens that adjusts the color signal that hits the human eye and the O2Amp was born.

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Filed under vision colour blindness glasses oxy-iso lenses science

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Chimps solve puzzles for the thrill of it

The apes, which are our closest relatives in the animal kingdom, seem to get the same level of satisfaction out of solving brain teasers as their human evolutionary cousins.


A study published by the Zoological Society of London shows that six chimpanzees who were given a game which involved moving red dice or Brazil through a maze of pipes enjoyed solving the puzzle whether they got a reward or not.


The researchers claim this suggests they got the same kind of psychological reward as humans get when solving problems.


Most problem solving witnessed in the animal kingdom, where animals use tools or navigate mazes, are with the aim of reaching food. Hyenas, octopuses and birds such as crows all show the ability to solve problems.


Chimpanzees have also been witnessed in the wild using tools such as a stick to forage for insects or honey in hard to reach places like tree stumps.
But ZSL researcher Fay Clark said their research said they could be motivated by more than just food.
She said: “We noticed that the chimps were keen to complete the puzzle regardless of whether or not they received a food reward.
"This strongly suggests they get similar feelings of satisfaction to humans who often complete brain games for a feel-good reward.”

Chimps solve puzzles for the thrill of it

The apes, which are our closest relatives in the animal kingdom, seem to get the same level of satisfaction out of solving brain teasers as their human evolutionary cousins.

A study published by the Zoological Society of London shows that six chimpanzees who were given a game which involved moving red dice or Brazil through a maze of pipes enjoyed solving the puzzle whether they got a reward or not.

The researchers claim this suggests they got the same kind of psychological reward as humans get when solving problems.

Most problem solving witnessed in the animal kingdom, where animals use tools or navigate mazes, are with the aim of reaching food. Hyenas, octopuses and birds such as crows all show the ability to solve problems.

Chimpanzees have also been witnessed in the wild using tools such as a stick to forage for insects or honey in hard to reach places like tree stumps.

But ZSL researcher Fay Clark said their research said they could be motivated by more than just food.

She said: “We noticed that the chimps were keen to complete the puzzle regardless of whether or not they received a food reward.

"This strongly suggests they get similar feelings of satisfaction to humans who often complete brain games for a feel-good reward.”

Filed under primates problem solving reward animal behavior cognitive challenge psychology neuroscience science

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