Neuroscience
Month
Scientists at Wake Forest Baptist Medical Center have taken the first steps to create neural-like stem cells from muscle tissue in animals. Details of the work are published in two complementary studies published in the September online issues of the journals Experimental Cell Research and Stem Cell Research.
“Reversing brain degeneration and trauma lesions will depend on cell therapy, but we can’t harvest neural stem cells from the brain or spinal cord without harming the donor,” said Osvaldo Delbono, M.D., Ph.D., professor of internal medicine at Wake Forest Baptist and lead author of the studies.
“Skeletal muscle tissue, which makes up 50 percent of the body, is easily accessible and biopsies of muscle are relatively harmless to the donor, so we think it may be an alternative source of neural-like cells that potentially could be used to treat brain or spinal cord injury, neurodegenerative disorders, brain tumors and other diseases, although more studies are needed.”
In an earlier study, the Wake Forest Baptist team isolated neural precursor cells derived from skeletal muscle of adult transgenic mice (PLOS One, Feb.3, 2011).
In the current research, the team isolated neural precursor cells from in vitro adult skeletal muscle of various species including non-human primates and aging mice, and showed that these cells not only survived in the brain, but also migrated to the area of the brain where neural stem cells originate.
Another issue the researchers investigated was whether these neural-like cells would form tumors, a characteristic of many types of stem cells. To test this, the team injected the cells below the skin and in the brains of mice, and after one month, no tumors were found.
“Right now, patients with glioblastomas or other brain tumors have very poor outcomes and relatively few treatment options,” said Alexander Birbrair, a doctoral student in Delbono’s lab and first author of these studies. “Because our cells survived and migrated in the brain, we may be able to use them as drug-delivery vehicles in the future, not only for brain tumors but also for other central nervous system diseases.”
In addition, the Wake Forest Baptist team is now conducting research to determine if these neural-like cells also have the capability to become functioning neurons in the central nervous system.
The unexpected survival of embryonic neurons transplanted into the brains of newborn mice in a series of experiments at the University of California, San Francisco (UCSF) raises hope for the possibility of using neuronal transplantation to treat diseases like Alzheimer’s, epilepsy, Huntington’s, Parkinson’s and schizophrenia.
The experiments, described this week in the journal Nature, were not designed to test whether embryonic neuron transplants could effectively treat any specific disease. But they provide a proof-of-principle that GABA-secreting interneurons, a type of brain cell linked to many different neurological disorders, can be added in significant numbers into the brain and can survive without affecting the population of endogenous interneurons.
The survival of these cells after transplantation in numbers far greater than expected came as a shock to the team, which was led by UCSF professor Arturo Alvarez-Buylla, PhD, and former UCSF graduate student Derek Southwell, MD, PhD.
The prevailing theory held that the survival of developing neurons is something like a game of musical chairs. The brain has limited capacity for these cells, forcing them to compete with each other for the few available slots. Only those that find a place to “sit” (and receive survival signals derived from other cell types) will survive when the music stops. The rest die a withering death.
A paper by Shizhong Han and colleagues in the current issue of Biological Psychiatry implicates a new gene in the risk for cannabis dependence. This gene, NRG1, codes for the ErbB4 receptor, a protein implicated in synaptic development and function.
The researchers set out to investigate susceptibility genes for cannabis dependence, as research has already shown that it has a strong genetic component.
To do this, they employed a multi-stage design using genetic data from African American and European American families. In the first stage, a linkage analysis, the strongest signal was identified in African Americans on chromosome 8p21. Then using a genome-wide association study dataset, they identified one genetic variant at NRG1 that showed consistent evidence for association in both African Americans and European Americans. Finally, they replicated the association of that same variant in an independent sample of African-Americans.
All together, the findings suggest that NRG1 may be a susceptibility gene for cannabis dependence.
An interesting feature of this paper is that these findings may also suggest a link between the genetics of schizophrenia and the genetics of cannabis dependence. NRG1 emerged into public awareness after a series of genetic studies implicated it in the heritable risk for schizophrenia. Subsequent studies in post-mortem brain tissue also suggested that the regulation of NRG1 was altered in the brains of individuals diagnosed with schizophrenia.
Thus, the current findings may help to explain the already established link between cannabis use and the risk for developing schizophrenia. A number of epidemiologic studies have attributed the association of cannabis use and schizophrenia to the effects of cannabis on the brain rather than a common genetic link between these two conditions.
"The current data provide a potentially important insight into the heritable risk for schizophrenia and raise the possibility that there are some common genetic contributions to these two disorders," commented Dr. John Krystal, Editor of Biological Psychiatry.
However, further research will be necessary to further confirm the role that NRG1 plays in cannabis dependence and the potential link between cannabis use and psychosis.
Scientists have proved a 60-year-old theory about how nerve signals are sent around the body at varying speeds as electrical impulses.
Researchers tested how these signals are transmitted through nerve fibres, which enables us to move and recognise sensations such as touch and smell.
The findings from the University of Edinburgh have validated an idea first proposed by Nobel laureate Sir Andrew Huxley.
It has been known for many years that an insulating layer – known as myelin – which surrounds nerve fibres is crucial in determining how quickly these signals are sent.
This insulating myelin is interrupted at regular intervals along the nerve by gaps called nodes.
Scientists, whose work was funded by the Wellcome Trust, have now proved that the longer the distance between nodes, the quicker the nerve fibres send signals down the nerves.
The theory that the distance between these gaps might affect the speed of electrical signals was first proposed by Sir Andrew Huxley, who won the Nobel Prize in 1963 for his work on electrical signalling in the nervous system, and who died earlier this year.
The study, published in the journal Current Biology, will help provide insight into what happens in people with nerve damage. It will also shed light on how nerves develop before and after birth.
Professor Peter Brophy, Director of the University of Edinburgh’s Centre for Neuroregeneration, said: “The study gives us greater insight into how the central and peripheral nervous systems work and what happens after nerves become injured. We know that peripheral nerves have the capacity to repair, but shorter lengths of insulation around the nerve fibres after repair affect the speed with which impulses are sent around the body.”
The researchers found that when the myelin reached a certain length, the speed with which nerves impulses were conducted reached a peak.
The study, carried out in mice, also confirmed that a protein – periaxin – plays a key role in regulating the length of myelin layers around nerve fibres.
Washington State University researchers have developed a new drug candidate that dramatically improves the cognitive function of rats with Alzheimer’s-like mental impairment.
Their compound, which is intended to repair brain damage that has already occurred, is a significant departure from current Alzheimer’s treatments, which either slow the process of cell death or inhibit cholinesterase, an enzyme believed to break down a key neurotransmitter involved in learning and memory development.
Such drugs, says Joe Harding, a professor in WSU’s College of Veterinary Medicine, are not designed to restore lost brain function, which can be done by rebuilding connections between nerve cells.
"This is about recovering function,” he says. "That’s what makes these things totally unique. They’re not designed necessarily to stop anything. They’re designed to fix what’s broken. As far as we can see, they work.”
Harding, College of Arts and Sciences Professor Jay Wright and other WSU colleagues report their findings in the online “Fast Forward” section of the Journal of Pharmacology and Experimental Therapeutics.
Three studies conducted as part of Wayne State University’s Systems Biology of Epilepsy Project (SBEP) could result in new types of treatment for the disease and, as a bonus, for behavioral disorders as well.
The SBEP started out with funds from the President’s Research Enhancement Fund and spanned neurology, neuroscience, genetics and computational biology. It since has been supported by multiple National Institutes of Health-funded grants aimed at identifying the underlying causes of epilepsy, and it is uniquely integrated within the Comprehensive Epilepsy Program at the Wayne State School of Medicine and the Detroit Medical Center.
Under the guidance of Jeffrey Loeb, M.D., Ph.D., associate director of the Center for Molecular Medicine and Genetics (CMMG) and professor of neurology, the project brings together researchers from different fields to create an interdisciplinary research program that targets the complex disease. The multifaceted program at Wayne State is like no other in the world, officials say, with two primary goals: improving clinical care and creating novel strategies for diagnosis and treatment of patients with epilepsy.
Scientists at the University of Bath are one step further to understanding the role of one of the proteins that causes the neurodegenerative disorder, Amyotrophic Lateral Sclerosis (ALS), also known as Motor Neurone Disease (MND).
The scientists studied a protein called angiogenin, which is present in the spinal cord and brain that protects neurones from cell death. Mutations in this protein have been found in sufferers of MND and are thought to play a key role in the progression of the condition.
MND triggers progressive weakness, muscle atrophy and muscle twitches and spasms. The disease affects around 5000 people in the UK.
The team of cell biologists and structural biologists have, for the first time, produced images of the 3D structures of 11 mutant versions of angiogenin to see how the mutations changed the structure of the active part of the molecule, damaging its function.
The study, published in the prestigious journal Nature Communications, provides insights into the causes of this disease and related conditions such as Parkinson’s Disease.
The team also looked at the effects of the malfunctioning proteins on neurones grown from embryonic stem cells in the laboratory.
They found that some of the mutations stopped the protein being transported to the cell nucleus, a process that is critical for the protein to function correctly.
The mutations also prevented the cells from producing stress granules, the neurone’s natural defence from stress caused by low oxygen levels.
Dr Vasanta Subramanian, Reader in Biology & Biochemistry at the University, said:
“This study is exciting because it’s the first time we’ve directly linked the structure of these faulty proteins with their effects in the cell.
“We’ve worked alongside Professor Ravi Acharya’s group to combine structural knowledge with cell biology to gain new insights into the causes of this devastating disease.
“We hope that the scientific community can use this new knowledge to help design new drugs that will bind selectively to the defective protein to protect the body from its damaging effects.”
The findings were welcomed by medical research charity, the Motor Neurone Disease (MND) Association, the only national charity in England, Wales and Northern Ireland dedicated to supporting people living with MND while funding and promoting cutting-edge global research to bring about a world free of the disease.
Dr Brian Dickie, Director of Research Development at the charity, said: “The researchers at the University of Bath have skilfully combined aspects of biology, chemistry and physics to answer some fundamental questions on how angiogenin can damage motor neurones. It not only advances our understanding of the disease, but may also give rise to new ideas on treatment development.”
A sudden and mysterious burst of activity originating in the retina of a developing fetus spurs brain connections that are essential to development of finely-tuned sight, Yale researchers report in the journal Nature. Interference with this spontaneous wave of activity could play a role in neurodevelopmental disorders such as autism, the scientists speculate.
The study in mice is the first to demonstrate in a living animal that this wave of activity spreads throughout large regions of the brain and is crucial to wiring of the visual system. Without the wiring, infants would not be able to distinguish details in their environment.
“If you interfere with this activity, the circuits are all messed up, the wiring details are all wrong,” said Michael Crair, the William Ziegler III Professor of Neurobiology and Professor of Ophthalmology and Visual Science and senior author of the study.
For instance, this activity might allow a newborn human baby to perceive such details as the five fingers attached to her hand or her mother’s face. This wave wires up the visual system so that infants are poised to learn from their environment soon after birth.
The development of animals from a fertilized egg into trillions of intricately connected and specialized cells is the result of a precisely timed expression of genes. However, the Nature paper introduces another necessary factor — a mysterious wave of activity arising in the retina itself that propagates through several regions of the brain. Crair terms this wave an emergent property, or a trait possessed by a complex system that cannot be directly traced to its individual parts. This experiment in living, neonatal mice shows that this wave is crucial to the proper wiring not only of the visual system but other brain areas as well.
Crair said his lab plans to explore whether interruptions of this activity might play a role in neurodevelopmental disorders such as autism or schizophrenia.
What does the neuroscientist Colin Blakemore make of an American neurosurgeon’s account of the afterlife?
Have you ever noticed that more people come back from Heaven than from Hell? We have all read those astonishing reports of near-death experiences (NDEs, as the aficionados call them) – the things that people say have happened to them when they almost, but don’t quite, shuffle off the coil.
They are nearly always pleasant and deeply reassuring in a saccharin-soaked way. Lots of spinning down warm, dark tunnels to the sound of celestial music; lots of trips along country lanes lined with hedges, towards the light of a welcoming cottage at the end of the road; lots of tumbling down Alice-in-Wonderland rabbit holes, but without the damaging effects of gravity.
True, Dr Maurice S Rawlings Jr, MD, heart surgeon in Chattanooga, Tennessee, and author of To Hell and Back, did have patients who reported very nasty NDEs after they came back on his operating table. Booming noises; licking flames and all that Mephistophelian stuff. But perhaps that tells us more about the challenges of living in Chattanooga, Tennessee, than about the metaphysics of life after death.
Predictably, the amazingly consistent, remarkably heaven-like experiences recounted by the majority of NDE-ers (yes, that really is what the experts call them) have been summarily dismissed by materialist sceptics – like me. Of course the brain does funny things when it’s running out of oxygen. The odd perceptions are just the consequences of confused activity in the temporal lobes.
But NDEs have taken on a new cloak of respectability with a book by a Harvard doctor. Proof of Heaven, by Eben Alexander, will make your toes wiggle or curl, depending on your prejudices. What’s special about his account of being dead is that he’s a neurosurgeon. At least that’s what the publicity is telling us. It’s a cover story in Newsweek magazine, with a screaming headline: “Heaven is Real: a doctor’s account of the afterlife”.
Scientists studying a rare genetic disorder have identified a molecular pathway that may play a role in schizophrenia, according to new research in the Oct. 10 issue of The Journal of Neuroscience. The findings may one day guide researchers to new treatment options for people with schizophrenia — a devastating disease that affects approximately 1 percent of the world’s population.
Schizophrenia is characterized by a multitude of symptoms, including hallucinations, social withdrawal, and learning and memory deficits, which usually appear during late adolescence or early adulthood. Efforts to identify disease causes have been complicated by the fact that no single genetic mutation is strongly associated with the disease. By studying a rare genetic disorder that increases the risk of schizophrenia, Laurie Earls, PhD, and colleagues in the laboratory of Stanislav Zakharenko, MD, PhD, at St. Jude Children’s Research Hospital identified molecular changes that affect memory and are also present in people with schizophrenia.
Approximately 30 percent of people with a genetic disorder known as 22q11 deletion syndrome develop schizophrenia, making it one of the strongest risk factors for the disease. In previous studies of mice with the 22q11 deletion, Zakharenko’s group identified changes in nerve cells leading to deficits in the hippocampus — the brain’s learning and memory center — that appear with age. In the current study, the group confirmed similar molecular changes occur in people with schizophrenia. They also zeroed in on the gene contributing to the nerve cell changes.
"This study makes some very important discoveries about the precise mechanisms underlying the learning and memory deficits seen in the genetic mouse model — problems that are a central part of the human disease," said Carrie Bearden, PhD, an expert on 22q11 deletion syndrome at the University of California, Los Angeles, who was not involved in the study. "Pinpointing the specific gene involved is the first step toward developing targeted therapies that could reverse the cognitive deficits associated with schizophrenia, both in the context of this genetic mutation and the broader population," she added.
In previous studies, Zakharenko’s group found that abnormal nerve cell communication and cognitive dysfunction was associated with elevated levels of a protein that regulates calcium in certain nerve cells known as Serca2. These abnormalities are only detectable with age in mice with the 22q11 deletion.
In the current study, the researchers identified the gene Dgcr8 as the source of the changes.It produces molecules called microRNAs that normally keep Serca2 in check. Without them, the protein becomes elevated.By adding these molecules back into the hippocampus of animals with the 22q11 deletion, the researchers were able to reduce elevated Serca2 levels and reduce the cellular deficits associated with this genetic defect.
To assess whether the findings from these genetic mouse studies might translate to schizophrenia, the authors analyzed post-mortem brain tissue from people with schizophrenia. The researchers discovered that Serca2 was elevated even in patients with schizophrenia who did not have the 22q11 deletion.
"These data suggest a link between the nerve cell changes in patients with the 22q11 deletion syndrome and those that occur in patients with schizophrenia," Zakharenko said. "Serca2 regulation represents a novel therapeutic target for schizophrenia."
Where the non-human animal research investigating reproduction-induced cognitive reorganization has focused on neural plasticity and adaptive advantage in response to the demands associated with pregnancy and parenting, human studies have primarily concentrated on pregnancy-induced memory decline. The current review updates Henry and Rendell’s 2007 meta-analysis, and examines cognitive reorganization as the result of reproductive experience from an adaptationist perspective. Investigations of pregnancy-induced cognitive change in human females may benefit by focusing on areas, such as social cognition, where a cognitive advantage would serve a protective function, and by extending the study duration beyond pregnancy into the postpartum period.
Results may help improve drugs for neurological disorders
Researchers have published the first highly detailed description of how neurotensin, a neuropeptide hormone which modulates nerve cell activity in the brain, interacts with its receptor. Their results suggest that neuropeptide hormones use a novel binding mechanism to activate a class of receptors called G-protein coupled receptors (GPCRs).
“The knowledge of how the peptide binds to its receptor should help scientists design better drugs,” said Dr. Reinhard Grisshammer, a scientist at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and an author of the study published in Nature.
Binding of neurotensin initiates a series of reactions in nerve cells. Previous studies have shown that neurotensin may be involved in Parkinson’s disease, schizophrenia, temperature regulation, pain, and cancer cell growth.
Dr. Grisshammer and his colleagues used X-ray crystallography to show what the receptor looks like in atomic detail when it is bound to neurotensin. Their results provide the most direct and detailed views describing this interaction which may change the way scientists develop drugs targeting similar neuropeptide receptors.
X-ray crystallography is a technique in which scientists shoot X-rays at crystallized molecules to determine a molecule’s shape and structure. The X-rays change directions, or diffract, as they pass through the crystals before hitting a detector where they form a pattern that is used to calculate the atomic structure of the molecule. These structures guide the way scientists think about how proteins work.
Neurotensin receptors and other GPCRs belong to a large class of membrane proteins which are activated by a variety of molecules, called ligands. Previous X-ray crystallography studies showed that smaller ligands, such as adrenaline and retinal, bind in the middle of their respective GPCRs and well below the receptor’s surface. In contrast, Dr. Grisshammer’s group found that neurotensin binds to the outer part of its receptor, just at the receptor surface. These results suggest that neuropeptides activate GPCRs in a different way compared to the smaller ligands.
Forming well-diffracting neuropeptide-bound GPCR crystals is very difficult. Dr. Grisshammer and his colleagues spent many years obtaining the results on the neurotensin receptor. During that time Dr. Grisshammer started collaborating with a group led by Dr. Christopher Tate, Ph.D. at the MRC Laboratory of Molecular Biology, Cambridge, England. Dr. Tate’s lab used recombinant gene technology to create a stable version of the neurotensin receptor which tightly binds neurotensin. Meanwhile Dr. Grisshammer’s lab employed the latest methods to crystallize the receptor bound to a short version of neurotensin.
The results published today are the first X-ray crystallography studies showing how a neuropeptide agonist binds to neuropeptide GPCRs. Nonetheless, more work is needed to fully understand the detailed signaling mechanism of this GPCR, said Dr. Grisshammer.
From pigeons that can recognise faces to a chimp that stores rocks to throw at visitors, all animals have memories. But how similar are they to ours?
(Image: Matt Jacob/Tendance Floue)
EVERY morning, you take a walk in the park, bringing some bread to feed the pigeons. As the days wear on, you begin to see the birds as individuals; you even start to name them. But what do the pigeons remember of you? Do they think kindly of you as they drop off to sleep at night, or is your face a blank, indistinguishable from the others strolling through the park?
These questions may seem whimsical, but knowing what other creatures recall is crucial if we are to understand their inner lives. It turns out that the range of mnemonic feats in the wild is nearly as varied as life itself.
If you take memory to mean any ability to store and respond to past events, even the simplest organisms meet the grade. Blobs of slime mould, for instance, which can slowly crawl across a surface, seem to note the timing of changes to their climate, slowing their movement in anticipation of an expected dry spell - even when it never actually arrives.
With the emergence of the first neurons about half a billion years ago, memories became more intricate as information could be stored in the patterns of electrical connections within the nervous system. This type of learning may have been behind the Cambrian explosion - the sudden appearance and rapid evolution of more complex species about 530 million years ago - because it enabled animals to exploit new niches, say Eva Jablonka at Tel Aviv University and Simona Ginsburg at the Open University of Israel.
Over the following few hundred million years, increasingly advanced skills could emerge with different forces driving the evolution of each creature’s mind. The result is a surprising range of mnemonic feats throughout the animal kingdom. Migratory cardinal fish, for instance, can remember where they laid their eggs during the breeding season and, after over-wintering in deep water, return to within half a metre of the same spot. Animals as diverse as lizards, bees and octopuses can learn the way out of a maze, and pigeons have an excellent visual recognition, learning to recognise more than a thousand different images. They can even recognise individual humans and aren’t fooled by a change of clothes.
Such skills, although impressive, don’t match our experiences of episodic memory, in which we immerse ourselves in specific events. A pigeon might learn to associate your face with food, but it probably can’t remember your last meeting in the way you might be able to recall details of your last trip to the park.
(Image credit: chichacha)
Recent studies have linked caffeine consumption to a reduced risk of Alzheimer’s disease, and a new University of Illinois study may be able to explain how this happens.
“We have discovered a novel signal that activates the brain-based inflammation associated with neurodegenerative diseases, and caffeine appears to block its activity. This discovery may eventually lead to drugs that could reverse or inhibit mild cognitive impairment,” said Gregory Freund, a professor in the U of I’s College of Medicine and a member of the U of I’s Division of Nutritional Sciences.
Freund’s team examined the effects of caffeine on memory formation in two groups of mice—one group given caffeine, the other receiving none. The two groups were then exposed to hypoxia, simulating what happens in the brain during an interruption of breathing or blood flow, and then allowed to recover.
The caffeine-treated mice recovered their ability to form a new memory 33 percent faster than the non-caffeine-treated mice. In fact, caffeine had the same anti-inflammatory effect as blocking IL-1 signaling. IL-1 is a critical player in the inflammation associated with many neurodegenerative diseases, he said.
“It’s not surprising that the insult to the brain that the mice experienced would cause learning memory to be impaired. But how does that occur?” he wondered.
The scientists noted that the hypoxic episode triggered the release of adenosine by brain cells.
“Your cells are little powerhouses, and they run on a fuel called ATP that’s made up of molecules of adenosine. When there’s damage to a cell, adenosine is released,” he said.
Just as gasoline leaking out of a tank poses a danger to everything around it, adenosine leaking out of a cell poses a danger to its environment, he noted.
The extracellular adenosine activates the enzyme caspase-1, which triggers production of the cytokine IL-1β, a critical player in inflammation, he said.
“But caffeine blocks all the activity of adenosine and inhibits caspase-1 and the inflammation that comes with it, limiting damage to the brain and protecting it from further injury,” he added.
Caffeine’s ability to block adenosine receptors has been linked to cognitive improvement in certain neurodegenerative diseases and as a protectant against Alzheimer’s disease, he said.
“We feel that our foot is in the door now, and this research may lead to a way to reverse early cognitive impairment in the brain. We already have drugs that target certain adenosine receptors. Our work now is to determine which receptor is the most important and use a specific antagonist to that receptor,” he said.
The study appears in the Journal of Neuroscience and can be viewed online at http://www.jneurosci.org/content/32/40/13945.full
McGill researchers link genetic mutation to psychiatric disease and obesity
Deletion of brain-derived neurotrophic factor leads to major depression, anxiety, and obesity
McGill researchers have identified a small region in the genome that conclusively plays a role in the development of psychiatric disease and obesity. The key lies in the genomic deletion of brain-derived neurotrophic factor, or BDNF, a nervous system growth factor that plays a critical role in brain development.
To determine the role of BDNF in humans, Prof. Carl Ernst, from McGill’s Department of Psychiatry, Faculty of Medicine, screened over 35,000 people referred for genetic screening at clinics and over 30,000 control subjects in Canada, the U.S., and Europe. Overall, five individuals were identified with BDNF deletions, all of whom were obese, had a mild-moderate intellectual impairment, and had a mood disorder. Children had anxiety disorders, aggressive disorders, or attention deficit-hyperactivity disorder (ADHD), while post-pubescent subjects had anxiety and major depressive disorders. Subjects gradually gained weight as they aged, suggesting that obesity is a long-term process when BDNF is deleted.
"Scientists have been trying to find a region of the genome which plays a role in human psychopathology, searching for answers anywhere in our DNA that may give us a clue to the genetic causes of these types of disorders," says Prof. Ernst, who is also a researcher at the Douglas Mental Health University Institute. "Our study conclusively links a single region of the genome to mood and anxiety."
The findings, published in the Archives of General Psychiatry, reveal for the first time the link between BDNF deletion, cognition, and weight gain in humans. BDNF has been suspected to have many functions in the brain based on animal studies, but no study had shown what happens when BDNF is missing from the human genome. This research provides a step toward better understanding human behaviour and mood by clearly identifying genes that may be involved in mental disorders.
"Mood and anxiety can be seen like a house of cards. In this case, the walls of the house represent the myriad of biological interactions that maintain the structure," says Ernst, "Studying these moving parts can be tricky, so teasing apart even a single event is important. Linking a deletion in BDNF conclusively to mood and anxiety really tells us that it is possible to dissect the biological pathways involved in determining how we feel and act.
We now have a molecular pathway we are confident is involved in psychopathology,” adds Ernst, “Because thousands of genes are involved in mood, anxiety, or obesity, it allows us to root our studies on a solid foundation. All of the participants in our study had mild-moderate intellectual disability, but most people with these cognitive problems do not have psychiatric problems – so what is it about deletion of BDNF that affects mood? My hope now is to test the hypothesis that boosting BDNF in people with anxiety or depression might improve brain health.”
How we manage to attend to multiple objects without being distracted by irrelevant information
The “tiki-taka”-style of the Spanish national football team is amazing to watch: Xavi passes to Andrès Iniesta, he just rebounds the ball once and it’s right at Xabi Alonso’s foot. The Spanish midfielders cross the field as if they run on rails, always maintaining attention on the ball and the teammates, the opponents chasing after them without a chance. An international team of scientists from the German Primate Center and McGill University in Canada, including Stefan Treue, head of the Cognitive Neuroscience Laboratory, has now uncovered how the human brain makes such excellence possible by dividing visual attention: The brain is capable of splitting its ‘attentional spotlight’ for an enhanced processing of multiple visual objects. (Neuron, doi: 10.1016/j.neuron.2011.10.013)
When we pay attention to an object, neurons responsible for this location in our field of view are more active then when they process unattended objects. But quite often we want to pay attention to multiple objects in different spatial positions, with interspersed irrelevant objects. Different theories have been proposed to account for this ability. One is, that the attentive focus is split spatially, excluding objects between the attentional spotlights. Another possibility is, that the attentional focus is zoomed out to cover all relevant objects, but including the interspersed irrelevant ones. A third possibility would be a single focus rapidly switching between the attended objects.
Studying rhesus macaques
In order to explain how such a complex ability is achieved, the neuroscientists measured the activity of individual neurons in areas of the brain involved in vision. They studied two rhesus macaques, which were trained in a visual attention task. The monkeys had learned to pay attention to two relevant objects on a screen, with an irrelevant object between them. The experiment showed, that the macaques’ neurons responded strongly to the two attended objects with only a weak response to the irrelevant stimulus in the middle. So the brain is able to spatially split visual attention and ignore the areas in between. “Our results show the enormous adaptiveness of the brain, which enables us to deal effectively with many different situations.
This multi-tasking allows us to simultaneously attend multiple objects”, Stefan Treue says. Such a powerful ability of our attentive system is one precondition for humans to become perfect football-artists but also to safely navigate in everyday traffic.