Neuroscience

The real culprits of colour blindness are vision cells rather than unusual wiring in the eye and brain, recent research has shown.

The discovery brings scientists a step closer to restoring full colour vision for people who are colour blind – a condition that affects close to two million Australians, says Professor Paul Martin from The Vision Centre and The University of Sydney.

It may also help pave the way for an answer to one of the most common causes of blindness – age-related macular degeneration (AMD), which accounts for half of the legal blindness cases in Australia.

“There are millions of cones in our eyes – vision cells that pick up bright light and allow us to see colour,” Prof. Martin says. “They are nicknamed red, green and blue cones because they are sensitive to different wavelengths of light.

“We now know that in the macular region of the eye, each cone has its own ’private line’ into the optic nerve and the brain. Just as a painter can mix from three tubes of paint to produce a wide and vivid palette, our brain uses the ‘private lines’ from the three cone types to create thousands of colour sensations.

Scientists previously thought that full colour vision depends on specialised nerve wiring in the eye and brain, but animal studies show that the wiring is identical for monkeys whether they have normal or abnormal colour vision, Prof. Martin says.

“This tells us that there’s nothing wrong in the brain – it’s only working with the signals that it receives on the ‘private lines’,” he says. “So the only difference in normal and abnormal colour vision is caused by the first stage of sight, which points to faulty cones. Either they have failed to develop, or else they are picking up abnormal wavelengths.

“Now that we know faulty wiring isn’t the cause, we can concentrate on fixing the cones, which are controlled by genes – and thus prone to mutation or mistakes during cell replication. There are already promising results from gene therapy as a way to restore full colour vision in colour blind monkeys.”

“While we have still have some way to go, the benefits of this gene therapy – if successful – can potentially extend beyond providing complete colour vision,” he says.

“If we can get these genes to work in human eyes, it means that the same approach might be possible for other visual problems – including blinding diseases such as macular degeneration.”

"In macular degeneration, energy supplies to the macula can’t keep up with demand. So the ‘private line’ system must be very energy-intensive. Gene therapy could be used to turn down the cones’ energy demand, or to increase energy supply from supporting cells to cone cells,” Prof. Martin says.

“Together with clinical researchers at the Save Sight Institute, we are now working hard to find out exactly how many ‘private lines’ there are in humans. That can point us to where energy demand is highest and we can target gene therapy to the right place.

"So animal research on ‘private lines’ for colour vision has given new clues for understanding one of the most important visual diseases – macular degeneration – in humans."

By Sabrina Richards | September 20, 2012

Researchers find that photoreceptors expressed in zebrafish hypothalamus contribute to light-dependent behavior.

Juvenile zebrafish.

Zebrafish larvae without eyes or pineal glands can still respond to light using photopigments located deep within their brains.  Published in Current Biology, the findings are the first to link opsins, photoreceptors located in the hypothalamus and other brain areas, to increased swimming in response to darkness, a behavior researchers hypothesize may help the fish move toward better-lit environments.

“[It’s a] strong demonstration that opsin-dependent photoreceptors in deep brain areas affect behaviors,” said Samer Hattar, who studies light reception in mammals at Johns Hopkins University but did not participate in the research.

Photoreceptors in eyes enable vision, and photoreceptors in the pineal gland, a small endocrine gland located in the center of the vertebrate brain, regulate circadian rhythms. But photoreceptors are also found in other brain areas of both invertebrates and vertebrate lineages. The function of these extraocular photoreceptors has been best studied in birds, where they regulate seasonal reproduction, explained Harold Burgess, a behavioral neurogeneticist at the Eunice Kennedy Shriver National Institute for Child Health and Human Development.

Many opsins have been reported in the brains of tiny and transparent larval zebrafish, raising the possibility that light could be stimulating the photoreceptors even deep in the brain. To test for behaviors that may be regulated by deep brain photoreceptors, Burgess and his colleagues in Wolfgang Driever’s lab at the University of Freiburg removed the eyes of zebrafish larvae, and compared their behavior to larvae that retained their eyes. Although most light-dependent behavior required eyes, the eyeless larvae did respond when the lights were turned off, increasing their activity for a several minutes, though to a somewhat lesser extent than control larvae. But the fact that they responded at all suggests that non-retinal photoreceptors contributed to the behavior.

To confirm the role of the deep brain photoreceptors, the researchers also tested eyeless larvae that had been genetically modified to block expression of photoreceptors in the pineal gland. This fish still showed this jump in activity for several minutes after entering darkness.

Two different types of opsins—melanopsin and multiple tissue opsin—are expressed in the same type of neuron in zebrafish hypothalamus. Burgess and his colleagues looked at zebrafish missing the transcription factor Orthopedia, which is unique to these neurons, and found that the darkness-induced activity boost is nearly absent in these fish. To further narrow the search for the responsible photoreceptors, the researchers overexpressed melanopsin in hypothalamus neurons that co-express Orthopedia and melanopsin, and found that it increased the sensitivity of eyeless zebrafish to reductions in light. The results point to both melanopsin and Orthopedia as key players in modulating this behavior and pinpoint the location to neurons that coexpress these factors in the zebrafish hypothalamus.

Interestingly, the hypothalamus is one of the oldest parts of the vertebrate brain, said Detlev Arendt, a developmental biologist at the European Molecular Biology Laboratory in Heidelberg. “It’s very possible that this is one of the oldest functions”—one that evolved in “non-visual organisms” that had no eyes but still needed to sense light.

Although not as directed and efficient as eye-dependent behaviors that help fish swim toward light, Burgess speculates that deep brain opsins can still benefit zebrafish larvae. “You could imagine situation where it can’t see light, if a leaf falls on it and it doesn’t know where to swim. I think this behavior puts it in a hyperactive state where it swims wildly for several minutes until it reaches enough light for eyes to take over,” he explained, noting that such behavior is common in invertebrates.

It remains to be seen whether these deep brain opsins regulate other behaviors, perhaps in similar fashion to seasonal hormonal regulation in birds, but Hattar believes it is likely. “It’s beyond reasonable doubt there are many functions for these deep brain photoreceptors.”

People with degenerative neurological conditions could benefit from research that shows why their brain cells stop communicating properly.

Scientists believe that the findings could help to develop treatments that slow the progress of a broad range of brain disorders such as Huntington’s, Alzheimer’s and Parkinson’s diseases.

The team at the University, led by Professor Tom Gillingwater, analysed how connection points between brain cells break down during disease and identified six proteins that control the process.

Sending Signals

When connection points in the brain, known as synapses, stop working - because of injury or disease - the chain of brain signalling breaks down and cannot be repaired.

The research from The Roslin Institute and Centre for Integrative Physiology at the University will help scientists identify drugs that target these proteins.

This could eventually enable clinicians to slow the progress of these disorders.

This study has identified key proteins that may control what goes wrong in a range of brain disorders. We now hope to identify drugs that prevent the breakdown of communication between brain cells and, as a result, halt the progress of these devastating neurodegenerative conditions. — Dr Thomas Wishart Career Track Fellow, The Roslin Institute at the University

Millions of Americans take antidepressants such as Prozac, Effexor, and Paxil, but the explanations for how they work never satisfied René Hen, a professor of psychiatry, neuroscience and pharmacology.

So the French-born researcher began a series of experiments a decade ago that are now helping to overturn conventional wisdom about the class of antidepressants known as selective serotonin reuptake inhibitors (SSRIs) and providing new insights into the biological mechanisms in the brain that affect mood and cognition.

Adult-born neurons in the hippocampus have been engineered to express channelrhodopsin (red), a protein that allows the activation of these neurons and the study of their impact on pattern separation and mood. (Image credit: Mazen Kheirbek and René Hen)

SSRIs, it has long been thought, work by inhibiting brain cells from reabsorbing serotonin, a signaling agent in the brain associated with positive mood. Yet unlike with psychoactive substances, the effects of the drugs take weeks to be felt—even though the increase in serotonin circulating in the brain begins almost immediately. Something more, Hen concluded, must be happening after that to create such a profound effect in depressed patients.

In 2003, Hen demonstrated an important finding in mice: The change in mood—measured by the amount of time it took the animals to overcome anxiety and feed in new environments—appeared to be due in part to the production of new brain cells in the hippocampus, an area of the brain associated with learning and memory. And those new brain cells, Hen thinks, are the result of growth-stimulating chemicals released in the brain, in response to the increased serotonin.

Last year, Hen published another groundbreaking study, suggesting how these new brain cells might affect mood. The new brain cells are located in the dentate gyrus, an area of the hippocampus involved in pattern separation, a cognitive process that helps us to recognize that something is new and different from similar experiences and stimuli. This information is then sent to other brain regions where the new stimulus is assigned a positive or negative emotional value.

Using genetic manipulations that block or enhance the production of brain cells in the dentate gyrus, Hen demonstrated that the new brain cells led to a marked improvement not just in the cognitive abilities of mice, but also in their mood. “What we think, even though it hasn’t been proven yet, is that some depressed human patients also have a problem with pattern separation,” Hen says. “What we are hoping is, if we can boost production of new neurons in their hippocampus, maybe we can improve pattern separation in patients and decrease general symptoms.”

Hen sees numerous ways that a disruption in pattern separation might lead to negative emotions such as anxiety and depression. The hippocampus is located next to, and is strongly linked with, another brain structure, the almond-shaped amygdala, thought to be the seat of our emotions.

If wrong judgments were assigned to novel stimuli in the amygdala, that could easily trigger the brain’s fight-or-flight instinct or, at the very least, produce fear. That might help explain features of anxiety disorders—why survivors of the 9/11 terrorist attacks suffering from post-traumatic stress disorder, for instance, might be hit with a panic attack whenever they see an airplane fly over a skyscraper, Hen says.

A deficit in pattern separation might also help explain why depressed patients often are unable to experience pleasure, exhibit a lack of interest in novel experiences, and feel profound malaise. Perhaps they are simply unable to register an experience as novel or pleasurable because they are unable to recognize it as sufficiently different from prior experiences.

Hen is quick to point out that new brain cell production in the hippocampus is just one effect of a cascade of neurochemical changes unleashed by SSRIs. Other researchers have demonstrated, among other things, that the drugs also have a strong impact on the prefrontal cortex, the area of the brain associated with executive functions such as decision-making and restraint.

Even so, Hen hopes his findings will have significant implications for some depressed patients—and perhaps even reveal why certain antidepressants work for some people and not others. Over the next several years, he plans to explore his hypotheses further by evaluating the pattern-separation abilities of depressed patients before and after they are treated with SSRIs.

“There is still a long way to go, but we are at least starting to provide a theoretical framework,” Hen says. “With complex disorders such as anxiety and depression, you are dealing with many parts of the brain. We think we have identified the biological basis for one of the symptoms present in a subgroup of patients, and maybe by targeting it, we will be able to help them.”

A new oral medication to treat patients in the early stages of multiple sclerosis has shown considerable promise in two clinical trials, researchers announced on Wednesday.

The medication is on track to become just the third oral drug available to M.S. patients, and potentially the safest and most effective, experts said. The second oral drug, called Aubagio, was approved just last week.

M.S. was virtually untreatable only two decades ago, but today nine “disease modifying” drugs are available for early-stage patients; a half-dozen more are in the late stages of development. Most patients in the early stage of the disease, a form called relapsing-remitting M.S., take drugs by injection.

The two new studies, published online in The New England Journal of Medicine, found that the drug BG-12, developed by Biogen Idec, reduced relapse rates in patients with relapsing M.S. by about 50 percent. The drug also significantly reduced the frequency of new brain lesions often associated with these attacks, and slowed the progression of disease compared with a placebo.

The studies were Phase 3 trials, a last step on the road to drug approval. The Food and Drug Administration is required to make a decision about the drug’s approval before the end of this year.

“This drug is clearly quite effective in managing disease and reducing disability, and the safety profile looks quite good,” said Timothy Coetzee, the chief research officer at the National Multiple Sclerosis Society, who was not involved in the studies.

Multiple sclerosis is often a progressive disease in which the immune system damages neurons in the brain and spinal cord. A majority of people with M.S. have relapsing-remitting M.S., characterized by flare-ups that cause lesions in the brain to develop and neurological symptoms to emerge or worsen. Eventually, more than half of patients develop a progressive form of M.S., leading to permanent disabilities.

Interferons, the drugs most commonly used in relapsing M.S., reduce relapses by about 30 percent, and have not been shown to slow the progression of the disease and disability. The newly approved Aubagio also reduces relapses by about 30 percent, and it has the advantage of being an oral drug.

Two drugs that are substantially more effective, Tysabri and Gilenya, come with serious risks including, in rare cases, death. They are used as second-line treatments when an initial approach fails, and patients require some monitoring.

In the new studies, called Define and Confirm, patients were randomized into two groups, taking 240 milligrams of BG-12 either twice or three times a day. Patients in a third group took a placebo. The combined results showed that the drug reduced the relapse rate by about 50 percent. There was minimal difference between the twice-daily and thrice-daily regimens.

Taking BG-12 twice a day reduced the number of new or newly enlarging brain lesions by 71 percent to 99 percent, depending on the type of lesion and the study. The Define study found a statistically significant 38 percent reduction in the progression to disability.

The most frequent side effects were a temporary flushing and warm feeling and gastrointestinal symptoms including nausea, diarrhea, cramping and vomiting. Though both types of side effects were common, they tended to diminish after the first few weeks of use and were tolerated by most patients.

BG-12 is an anti-inflammatory that works by protecting nerves against injury. It is a fumaric acid, very similar to one widely used in Germany for the treatment of psoriasis. “The safety track record is well known and appears to be very strong,” said Dr. Robert Fox, lead author of one of the two new studies and medical director of the Mellen Center for Multiple Sclerosis Treatment and Research at the Cleveland Clinic.

“It’s a bright day for M.S. patients, but there is a gray cloud in that we still don’t have anything for those with progressive M.S.,” he added.

Delirium is widespread among older people but often goes ignored and untreated, according to new research by US and UK researchers including the University of East Anglia.

Published in the September issue of the Journal of Hospital Medicine, the findings show that delirium - or acute confusion – is common among older adults in hospitals and nursing homes. It has a negative impact on cognition and independence, significantly increases the risk of developing dementia, and triples the likelihood of death. Yet this common, acute condition is frequently either undiagnosed or accepted as inevitable.

Led by the Regenstrief Institute and Indiana University, the research team reviewed 45 years of research encompassing 585 studies. They found that one in three cases of delirium were preventable and are calling for delirium to be identified and treated early to prevent poor long-term prognosis.

“As a geriatric psychiatrist I have seen that around 50 per cent or people with dementia in hospital develop delirium,” said co-author Dr Chris Fox, of Norwich Medical School at the University of East Anglia.

“This is because in addition to having dementia, they have multiple risk factors that can predispose and precipitate delirium – including serious illnesses and pre-existing cognitive impairment. In addition, hospital staff commonly label the signs as dementia related and do not pick up the delirium.”

“We need to develop better mechanisms for diagnosing delirium so that prompt treatment regimes can be initiated.”

In general patient groups, more than 60 per cent of delirium cases are not recognised or treated, and significant numbers of elderly patients leave hospital with ongoing delirium which has been missed.

The authors, led by Dr Babar Khan of the Regenstrief Institute and Indiana University School of Medicine, said that delirium could be prevented by eliminating restraints, treating depression, ensuring that patients have access to glasses and hearing aids, and prescribing classes of antipsychotics that do not negatively affect the aging brain. They also noted the need for a more sensitive screening tool for delirium, especially when administered by a non-expert.

“Delirium is extremely common among older adults in intensive care units and is not uncommon in other hospital units and in nursing homes, but too often it is ignored or accepted as inevitable,” said Dr Khan. “Delirium significantly increases risk of developing dementia and triples likelihood of death. It cannot be ignored.”

Co-author Dr Malaz Boustani, of the Regenstrief Institute, Indiana University School of Medicine and Wishard Healthy Aging Brain Center, said: “Having delirium prolongs the length of a hospital stay, increases the risk of post-hospitalization transfer to a nursing home, increases the risk of death and may lead to permanent brain damage.”

Contrary to the prevailing theories that music and language are cognitively separate or that music is a byproduct of language, theorists at Rice University’s Shepherd School of Music and the University of Maryland, College Park (UMCP) advocate that music underlies the ability to acquire language.

“Spoken language is a special type of music,” said Anthony Brandt, co-author of a theory paper published online this month in the journal Frontiers in Cognitive Auditory Neuroscience. “Language is typically viewed as fundamental to human intelligence, and music is often treated as being dependent on or derived from language. But from a developmental perspective, we argue that music comes first and language arises from music.”

Brandt, associate professor of composition and theory at the Shepherd School, co-authored the paper with Shepherd School graduate student Molly Gebrian and L. Robert Slevc, UMCP assistant professor of psychology and director of the Language and Music Cognition Lab.

“Infants listen first to sounds of language and only later to its meaning,” Brandt said. He noted that newborns’ extensive abilities in different aspects of speech perception depend on the discrimination of the sounds of language – “the most musical aspects of speech.”

The paper cites various studies that show what the newborn brain is capable of, such as the ability to distinguish the phonemes, or basic distinctive units of speech sound, and such attributes as pitch, rhythm and timbre.

The authors define music as “creative play with sound.” They said the term “music” implies an attention to the acoustic features of sound irrespective of any referential function. As adults, people focus primarily on the meaning of speech. But babies begin by hearing language as “an intentional and often repetitive vocal performance,” Brandt said. “They listen to it not only for its emotional content but also for its rhythmic and phonemic patterns and consistencies. The meaning of words comes later.”

Brandt and his co-authors challenge the prevailing view that music cognition matures more slowly than language cognition and is more difficult. “We show that music and language develop along similar time lines,” he said.

Infants initially don’t distinguish well between their native language and all the languages of the world, Brandt said. Throughout the first year of life, they gradually hone in on their native language. Similarly, infants initially don’t distinguish well between their native musical traditions and those of other cultures; they start to hone in on their own musical culture at the same time that they hone in on their native language, he said.

The paper explores many connections between listening to speech and music. For example, recognizing the sound of different consonants requires rapid processing in the temporal lobe of the brain. Similarly, recognizing the timbre of different instruments requires temporal processing at the same speed — a feature of musical hearing that has often been overlooked, Brandt said.

“You can’t distinguish between a piano and a trumpet if you can’t process what you’re hearing at the same speed that you listen for the difference between ‘ba’ and ‘da,’” he said. “In this and many other ways, listening to music and speech overlap.” The authors argue that from a musical perspective, speech is a concert of phonemes and syllables.

“While music and language may be cognitively and neurally distinct in adults, we suggest that language is simply a subset of music from a child’s view,” Brandt said. “We conclude that music merits a central place in our understanding of human development.”

Brandt said more research on this topic might lead to a better understanding of why music therapy is helpful for people with reading and speech disorders. People with dyslexia often have problems with the performance of musical rhythm. “A lot of people with language deficits also have musical deficits,” Brandt said.

More research could also shed light on rehabilitation for people who have suffered a stroke. “Music helps them reacquire language, because that may be how they acquired language in the first place,” Brandt said.

Misfolded proteins can cause various neurodegenerative diseases such as spinocerebellar ataxias (SCAs) or Huntington’s disease, which are characterized by a progressive loss of neurons in the brain. Researchers of the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch, Germany, together with their colleagues of the Université Paris Diderot, Paris, France, have now identified 21 proteins that specifically bind to a protein called ataxin-1. Twelve of these proteins enhance the misfolding of ataxin-1 and thus promote the formation of harmful protein aggregate structures, whereas nine of them prevent the misfolding (PLoS Genetics).

Proteins only function properly when the chains of amino acids, from which they are built, fold correctly. Misfolded proteins can be toxic for the cells and assemble into insoluble aggregates together with other proteins. Ataxin-1, the protein that the researchers have now investigated, is very prone to misfolding due to inherited gene defects that cause neurodegenerative diseases. The reason for this is that the amino acid glutamine is repeated in the amino acid chain of ataxin-1 very often - the more glutamine, the more toxic the protein. Approximately 40 repeats of glutamine are considered to be toxic for the cells.

Now, Dr. Spyros Petrakis, Dr. Miguel Andrade, Professor Erich Wanker and colleagues have identified 21 proteins that mainly interact with ataxin-1 and influence its folding or misfolding. Twelve of these proteins enhance the toxicity of ataxin-1 for the nerve cells, whereas nine of the identified proteins reduce its toxicity.

Furthermore, the researchers detected a common feature in the structure of those proteins that enhances toxicity and aggregation. It is a special structure scientists call “coiled-coil-domain” because it resembles a double twisted spiral or helix. Apparently this structure promotes aggregation, because proteins that interact with ataxin-1 and have this domain enhance the toxic effect of mutated ataxin-1. As the researchers said, this structure could be a potential target for therapy: “A careful analysis of the molecular details could help to discover drugs that suppress toxic processes.”

Scientists at Washington University School of Medicine in St. Louis have taken one of the first detailed looks into how Alzheimer’s disease disrupts coordination among several of the brain’s networks. The results, reported in The Journal of Neuroscience, include some of the earliest assessments of Alzheimer’s effects on networks that are active when the brain is at rest.

“Until now, most research into Alzheimer’s effects on brain networks has either focused on the networks that become active during a mental task, or the default mode network, the primary network that activates when a person is daydreaming or letting the mind wander,” says senior author Beau Ances, MD, assistant professor of neurology. “There are, however, a number of additional networks besides the default mode network that become active when the brain is idling and could tell us important things about Alzheimer’s effects.”

Ances and his colleagues analyzed brain scans of 559 subjects. Some of these subjects were cognitively normal, while others were in the early stages of very mild to mild Alzheimer’s disease. Scientists found that all of the networks they studied eventually became impaired during the initial stages of Alzheimer’s.

“Communications within and between networks are disrupted, but it doesn’t happen all at once,” Ances says. “There’s even one network that has a momentary surge of improved connections before it starts dropping again. That’s the salience network, which helps you determine what in your environment you need to pay attention to.”

Other networks studied by the researchers included:

• the dorsal attention network, which directs attention toward things in the environment that are salient;

• the control network, believed to be active in consciousness and decision-making; and

• the sensory-motor network, which integrates the brain’s control of body movements with sensory feedback (e.g., did the finger that just moved strike the right piano key?).

Scientists also examined Alzheimer’s effects on a brain networking property known as anti-correlations. Researchers identify networks by determining which brain areas frequently become active at the same time, but anti-correlated networks are noteworthy for the way their activities fluctuate: when one network is active, the other network is quiet. This ability to switch back-and-forth between networks is significantly diminished in participants with mild to moderate Alzheimer’s disease.

The default mode network, previously identified as one of the first networks to be impaired by Alzheimer’s, is a partner in two of the three pairs of anti-correlated networks scientist studied.

“While we can’t prove this yet, one hypothesis is that as things go wrong in the processing of information in the default mode network, that mishandled data is passed on to other networks, where it creates additional problems,” Ances says.

It’s not practical to use these network breakdowns to clinically diagnose Alzheimer’s disease, Ances notes, but they may help track the development of the disease and aid efforts to better understand its spread through the brain.

Ances plans to look at other markers for Alzheimer’s disease in the same subjects, such as levels in the cerebrospinal fluid of amyloid beta, a major component of Alzheimer’s plaques.

MRI brain scans no longer just show the various regions of brain activity; nowadays the networks in the brain can now be imaged with ever greater precision. This will make functional MRI (fMRI) increasingly powerful in the coming years, leading to tools that can be used in cognitive neuroscience. This is the claim made by Prof. David Norris in his inaugural lecture as Professor of Neuroimaging at the University of Twente on 13 September.

During the twenty years since the invention of fMRI (functional Magnetic Resonance Imaging) developments have come thick and fast, from initially identifying active brain regions to more complex analysis of the connections and hubs in the brain. In his inaugural lecture Norris describes how this has been achieved thanks to not only a growing understanding of the underlying biophysics but also rapid technological developments: scanners with larger magnetic fields, better image-processing techniques and algorithms. His aim is to go beyond merely localizing which parts of the brain are active. The challenge is to answer two questions: How are the various regions interconnected, structurally and functionally? What do the networks in our brains look like?

Faster and more powerful

Back in the 19^th century scientists observed increased blood flow in brain regions that are functionally active. fMRI enables the change in oxygen content to be seen. Haemoglobin, the substance that transports oxygen in the blood, can take the form of oxyhaemoglobin (when it is still combined with oxygen) and deoxyhaemoglobin (when the oxygen has been released), each of which has different magnetic properties. One of the complicating factors when interpreting the scans is that various physiological mechanisms are at work simultaneously, causing the deoxyhaemoglobin level to rise and fall. One of the remedies to increase accuracy, Norris explains, has been to increase the magnetic field strength: there are now MRI scanners operating at 7 Tesla. At the same time the speed at which laminae can be imaged has gone up by leaps and bounds: the entire brain can be scanned in three seconds with a precision of 1 millimetre.

Hubs

The functional connections between parts of the brain can be registered by means of blood flow, but MRI also enables the structural and anatomical connections to be seen. This involves measuring the movement of water molecules caused by the ‘white matter’ in nerve fibres. This technology is known as diffusion-weighted imaging (DWI). Combining these technologies provides a wealth of fresh information on the networks in the brain and the places where many connections come together, the ‘hubs’. Not only have ‘known networks’ thus been proven, so have networks that neuroscience posits as plausible but that have never been measured.

Image showing the distribution of connector hubs on the surface of a flattened brain. The top two figures show the medial views of each hemisphere, the bottom two show the external views.

CMI

The new Centre for Medical Imaging that is to come to the University of Twente campus will soon provide extensive facilities for collaborating in the field of fMRI, says Norris, who is also on the staff of the Donders Institute in Nijmegen.