Posts tagged science

April 2nd, 2012

Therapy to mend parts of the brain damaged by strokes has moved a step closer, thanks to research at Monash University’s Australian Regenerative Medicine Institute (ARMI) and the Florey Neuroscience Institutes (FNI).

Scientists, James Bourne and Jihane Homman-Ludiye, of ARMI, and Tobias Merson, of FNI, have discovered precursor cells in the visual processing region of the brains of young marmoset monkeys which can form new brain cells in a culture dish.

The work, published recently in the journal, PLoS One, raises the possibility of new therapies for victims of brain injuries such as stroke.

Commenting on the work, Stem Cells Australia’s Professor Martin Pera said “These results, which point strongly to the existence of stem cells in the primate cortex, have important implications for understanding normal brain function and add to a growing body of evidence that stem or progenitor cells may participate in the repair of injuries to this critical region of the brain.”

The team isolated a type of cell from the brain tissue of two-week-old marmoset monkeys, which have similar brains to humans.

They exposed the cells to various combinations of growth factors – proteins that promote cell proliferation – to see if the cells would multiply and form neurons in the culture dish.

Some of the cells started to multiply to form clusters of cells called neurospheres – the forerunners of mature brain cells – when treated with two specific growth factors. This puts them in a class of cells called neural progenitors. Like stem cells, these cells can convert into specialist cells to form various tissues.

It was once thought that our full complement of brain cells was fixed at birth. That view has been toppled in recent decades with the discovery of stem cells in the human brain that can form new neurons in adulthood, said Dr Merson, a neuroscientist.

But until now, those cells have been thought to be limited to two regions of the brain, including the hippocampus, which is involved in memory and learning.

The team’s breakthrough suggests that cells with the ability to form new neurons after birth are much more widespread in the brain. The cells under investigation in this latest research were isolated from the primary visual cortex, the brain structure at the back of the head involved in the processing of stimuli from the eyes. “This structure is very big in humans and other primates and is often affected by brain injury,” Dr Bourne said.

“Our results support the view that this region of the brain has the potential to generate new neurons at later stages than once thought,” Dr Merson said. “We were surprised at how easily we were able to generate the proliferating neurospheres. We were able to propagate them, and keep them in culture for up to a year.”

He said other regions of the brain involved in sensory processing could harbour similar cells.

The scientists plan further research to see if the production of new neurons after birth occurs naturally in the primary visual cortex, and whether the mechanism could be activated after injury.

“It could be plausible to manipulate the progenitor cells to produce more neurons,” Dr Bourne said.

Source: Neuroscience News

ScienceDaily (Apr. 2, 2012) — Scientists from the Florida campus of The Scripps Research Institute have shown in animal models that the loss of memory that comes with aging is not necessarily a permanent thing.

In a new study published this week in an advance, online edition of the journal Proceedings of the National Academy of Science, Ron Davis, chair of the Department of Neuroscience at Scripps Florida, and Ayako Tonoki-Yamaguchi, a research associate in Davis’s lab, took a close look at memory and memory traces in the brains of both young and old fruit flies.

What they found is that like other organisms — from mice to humans — there is a defect that occurs in memory with aging. In the case of the fruit fly, the ability to form memories lasting a few hours (intermediate-term memory) is lost due to age-related impairment of the function of certain neurons. Intriguingly, the scientists found that stimulating those same neurons can reverse these age-related memory defects.

"This study shows that once the appropriate neurons are identified in people, in principle at least, one could potentially develop drugs to hit those neurons and rescue those memories affected by the aging process," Davis said. "In addition, the biochemistry underlying memory formation in fruit flies is remarkably conserved with that in humans so that everything we learn about memory formation in flies is likely applicable to human memory and the disorders of human memory."

While no one really understands what is altered in the brain during the aging process, in the current study the scientists were able to use functional cellular imaging to monitor the changes in the fly’s neuron activity before and after learning.

"We are able to peer down into the fly brain and see changes in the brain," Davis said. "We found changes that appear to reflect how intermediate-term memory is encoded in these neurons."

Olfactory memory, which was used by the scientists, is the most widely studied form of memory in fruit flies — basically pairing an odor with a mild electric shock. These tactics produce short-term memories that persist for around a half-hour, intermediate-term memory that lasts a few hours, and long-term memory that persists for days.

The team found that in aged animals, the signs of encoded memory were absent after a few hours. In that way, the scientists also learned exactly which neurons in the fly are altered by aging to produce intermediate-term memory impairment. This advance, Davis notes, should greatly help scientists understand how aging alters neuronal function.

Intriguingly, the scientists took the work a step further and stimulated these neurons to see if the memory could be rescued. To do this, the scientists placed either cold-activated or heat-activated ion channels in the neurons known to become defective with aging and then used cold or heat to stimulate them. In both cases, the intermediate-term memory was successfully rescued.

Source: Science Daily

ScienceDaily (Apr. 2, 2012) — An international team of researchers involving the University of Adelaide has made a major discovery that could lead to more effective treatment of severe pain using morphine.

Morphine is an extremely important drug for pain relief, but it can lead to a range of side-effects — such as patients developing tolerance to morphine and increased sensitivity to pain. Until now, how this occurs has remained a mystery.

The team from the University of Colorado and University of Adelaide has shown for the first time how opioid drugs, such as morphine, create an inflammatory response in the brain — by activating an immune receptor in the brain.

They have also demonstrated how this brain immune receptor can be blocked, laying the groundwork for the development of new therapeutic drugs that improve the effectiveness of morphine while reducing many of its problematic side effects.

The results of this research are published April 2 in the Proceedings of the National Academy of Sciences (PNAS).

"Because morphine is considered to be such an important drug in the management of moderate to severe pain in patients right around the world, we believe these results will have far-reaching benefits," says study co-author Dr Mark Hutchinson, ARC Research Fellow in the University of Adelaide’s School of Medical Sciences.

Dr Hutchinson’s team, including University of Adelaide colleague Professor Andrew Somogyi, conducted studies in mice to validate the work done at the University of Colorado by the teams of Assistant Professor Hubert Yin and Professor Linda Watkins.

"For some time it’s been assumed that the inflammatory response from morphine was being caused via the classical opioid receptors," says Dr Hutchinson.

"However, we found instead that morphine binds to an immune receptor complex called toll-like receptor 4 (TLR4), and importantly this occurs in a very similar way to how this receptor detects bacteria.

"Our experiments in mice have shown that if this relationship with the immune receptor is disrupted, it will prevent the inflammatory response.

"This is an exciting result because it opens up possibilities for future drugs that promote the beneficial actions of morphine while negating some of the harmful side effects. This could lead to major advances in patient and palliative care," he says.

Source: Science Daily

ScienceDaily (Apr. 2, 2012) — As computer scientists this year celebrate the 100_th anniversary of the birth of the mathematical genius Alan Turing, who set out the basis for digital computing in the 1930s to anticipate the electronic age, they still quest after a machine as adaptable and intelligent as the human brain.

Now, computer scientist Hava Siegelmann of the University of Massachusetts Amherst, an expert in neural networks, has taken Turing’s work to its next logical step. She is translating her 1993 discovery of what she has dubbed “Super-Turing” computation into an adaptable computational system that learns and evolves, using input from the environment in a way much more like our brains do than classic Turing-type computers. She and her post-doctoral research colleague Jeremie Cabessa report on the advance in the current issue of Neural Computation.

"This model is inspired by the brain," she says. "It is a mathematical formulation of the brain’s neural networks with their adaptive abilities." The authors show that when the model is installed in an environment offering constant sensory stimuli like the real world, and when all stimulus-response pairs are considered over the machine’s lifetime, the Super Turing model yields an exponentially greater repertoire of behaviors than the classical computer or Turing model. They demonstrate that the Super-Turing model is superior for human-like tasks and learning.

"Each time a Super-Turing machine gets input it literally becomes a different machine," Siegelmann says. "You don’t want this for your PC. They are fine and fast calculators and we need them to do that. But if you want a robot to accompany a blind person to the grocery store, you’d like one that can navigate in a dynamic environment. If you want a machine to interact successfully with a human partner, you’d like one that can adapt to idiosyncratic speech, recognize facial patterns and allow interactions between partners to evolve just like we do. That’s what this model can offer."

Classical computers work sequentially and can only operate in the very orchestrated, specific environments for which they were programmed. They can look intelligent if they’ve been told what to expect and how to respond, Siegelmann says. But they can’t take in new information or use it to improve problem-solving, provide richer alternatives or perform other higher-intelligence tasks.

In 1948, Turing himself predicted another kind of computation that would mimic life itself, but he died without developing his concept of a machine that could use what he called “adaptive inference.” In 1993, Siegelmann, then at Rutgers, showed independently in her doctoral thesis that a very different kind of computation, vastly different from the “calculating computer” model and more like Turing’s prediction of life-like intelligence, was possible. She published her findings in Science and in a book shortly after.

"I was young enough to be curious, wanting to understand why the Turing model looked really strong," she recalls. "I tried to prove the conjecture that neural networks are very weak and instead found that some of the early work was faulty. I was surprised to find out via mathematical analysis that the neural models had some capabilities that surpass the Turing model. So I re-read Turing and found that he believed there would be an adaptive model that was stronger based on continuous calculations."

Each step in Siegelmann’s model starts with a new Turing machine that computes once and then adapts. The size of the set of natural numbers is represented by the notation aleph-zero, ℵ₀, representing also the number of different infinite calculations possible by classical Turing machines in a real-world environment on continuously arriving inputs. By contrast, Siegelmann’s most recent analysis demonstrates that Super-Turing computation has 2^ℵ0, possible behaviors. “If the Turing machine had 300 behaviors, the Super-Turing would have 2³⁰⁰, more than the number of atoms in the observable universe,” she explains.

The new Super-Turing machine will not only be flexible and adaptable but economical. This means that when presented with a visual problem, for example, it will act more like our human brains and choose salient features in the environment on which to focus, rather than using its power to visually sample the entire scene as a camera does. This economy of effort, using only as much attention as needed, is another hallmark of high artificial intelligence, Siegelmann says.

"If a Turing machine is like a train on a fixed track, a Super-Turing machine is like an airplane. It can haul a heavy load, but also move in endless directions and vary its destination as needed. The Super-Turing framework allows a stimulus to actually change the computer at each computational step, behaving in a way much closer to that of the constantly adapting and evolving brain," she adds.

Siegelmann and two colleagues recently were notified that they will receive a grant to make the first ever Super-Turing computer, based on Analog Recurrent Neural Networks. The device is expected to introduce a level of intelligence not seen before in artificial computation.

Source: Science Daily

ScienceDaily (Apr. 2, 2012) — Testosterone, the primary male sex hormone, appears to have antidepressant properties, but the exact mechanisms underlying its effects have remained unclear. Nicole Carrier and Mohamed Kabbaj, scientists at Florida State University, are actively working to elucidate these mechanisms.

They’ve discovered that a specific pathway in the hippocampus, a brain region involved in memory formation and regulation of stress responses, plays a major role in mediating testosterone’s effects, according to their new report in Biological Psychiatry.

Compared to men, women are twice as likely to suffer from an affective disorder like depression. Men with hypogonadism, a condition where the body produces no or low testosterone, also suffer increased levels of depression and anxiety. Testosterone replacement therapy has been shown to effectively improve mood.

Although it may seem that much is already known, it is of vital importance to fully characterize how and where these effects are occurring so that scientists can better target the development of future antidepressant therapies.

To advance this goal, the scientists performed multiple experiments in neutered adult male rats. The rats developed depressive-like behaviors that were reversed with testosterone replacement.

They also “identified a molecular pathway called MAPK/ERK2 (mitogen activated protein kinase/ extracellular regulated kinase 2) in the hippocampus that plays a major role in mediating the protective effects of testosterone,” said Kabbaj.

This suggests that the proper functioning of ERK2 is necessary before the antidepressant effects of testosterone can occur. It also suggests that this pathway may be a promising target for antidepressant therapies.

Kabbaj added, “Interestingly, the beneficial effects of testosterone were not associated with changes in neurogenesis (generation of new neurons) in the hippocampus as it is the case with other classical antidepressants like imipramine (Tofranil) and fluoxetine (Prozac).”

In results published elsewhere by the same group, testosterone has shown beneficial effects only in male rats, not in female rats.

Source: Science Daily

ScienceDaily (Apr. 2, 2012) — Why do some persons succumb to post-traumatic stress disorder (PTSD) while others who suffered the same ordeal do not? A new UCLA study sheds light on the answer.

UCLA scientists have linked two genes involved in serotonin production to a higher risk of developing PTSD. Published in the April 3 online edition of the Journal of Affective Disorders, the findings suggest that susceptibility to PTSD is inherited, pointing to new ways of screening for and treating the disorder.

"People can develop post-traumatic stress disorder after surviving a life-threatening ordeal like war, rape or a natural disaster," explained lead author Dr. Armen Goenjian, a research professor of psychiatry at the Semel Institute for Neuroscience and Human Behavior at UCLA. "If confirmed, our findings could eventually lead to new ways to screen people at risk for PTSD and target specific medicines for preventing and treating the disorder."

PTSD can arise following child abuse, terrorist attacks, sexual or physical assault, major accidents, natural disasters or exposure to war or combat. Symptoms include flashbacks, feeling emotionally numb or hyper-alert to danger, and avoiding situations that remind one of the original trauma.

Goenjian and his colleagues extracted the DNA of 200 adults from several generations of 12 extended families who suffered PTSD symptoms after surviving the devastating 1988 earthquake in Armenia.

In studying the families’ genes, the researchers found that persons who possessed specific variants of two genes were more likely to develop PTSD symptoms. Called TPH1 and TPH2, these genes control the production of serotonin, a brain chemical that regulates mood, sleep and alertness — all of which are disrupted in PTSD.

"We suspect that the gene variants produce less serotonin, predisposing these family members to PTSD after exposure to violence or disaster," said Goenjian. "Our next step will be to try and replicate the findings in a larger, more heterogeneous population."

Affecting about 7 percent of Americans, PTSD has become a pressing health issue for a large percentage of war veterans returning from Iraq and Afghanistan. The UCLA team’s discovery could be used to help screen persons who may be at risk for developing PTSD.

"A diagnostic tool based upon TPH1 and TPH2 could enable military leaders to identify soldiers who are at higher risk of developing PTSD, and reassign their combat duties accordingly," observed Goenjian. "Our findings may also help scientists uncover alternative treatments for the disorder, such as gene therapy or new drugs that regulate the chemicals responsible for PTSD symptoms."

According to Goenjian, pinpointing genes connected with PTSD symptoms will help neuroscientists classify the disorder based on brain biology instead of clinical observation. Psychiatrists currently rely on a trial and error approach to identify the best medication for controlling an individual patient’s symptoms.

Serotonin is the target of the popular antidepressants known as SSRIs, or selective serotonin re-uptake inhibitors, which prolong the effect of serotonin in the brain by slowing its absorption by brain cells. More physicians are prescribing SSRIs to treat psychiatric disease beyond depression, including PTSD and obsessive compulsive disorder.

Source: Science Daily

April 1, 2012

Rutgers scientists think they have found a way to prevent and possibly reverse the most debilitating symptoms of a rare, progressive childhood degenerative disease that leaves children with slurred speech, unable to walk, and in a wheelchair before they reach adolescence.

In today’s online edition of Nature Medicine, Karl Herrup, chair of the Department of Cell Biology and Neuroscience in the School of Arts and Sciences provides new information on why this genetic disease attacks the cerebellum – a part of the brain that controls movement coordination, equilibrium, and muscle tone – and other regions of the brain.

Using mouse and human brain tissue studies, Herrup and his colleagues at Rutgers found that in the brain tissue of young adults who died from ataxia-telangiectasia, or A-T disease, a protein known as HDAC4 was in the wrong place. HDAC4 is known to regulate bone and muscle development, but it is also found in the nerve cells of the brain. The protein that is defective in A-T, they discovered, plays a critical role in keeping HDAC4 from ending up in the nucleus of the nerve cell instead of in the cytoplasm where it belongs. In a properly working nerve cell, the HDAC4 in the cytoplasm helps to prevent nerve cell degeneration; however, in the brain tissue of young adults who had died from A-T disease, the protein was in the nucleus where it attacked the histones – the small proteins that coat and protect the DNA.

"What we have found is a double-edged sword," said Herrup. "While the HDAC4 protein protected a neuron’s function when it was in the cytoplasm, it was lethal in the nucleus."

To prove this point, Rutgers scientists analyzed mice, genetically engineered with the defective protein found in children with A-T, as well as wild mice. The animals were tested on a rotating rod to measure their motor coordination. While the normal mice were able to stay on the rod without any problems for five to six minutes, the mutant mice fell off within 15 to 20 seconds.

After being treated with trichostation A (TSA), a chemical compound that inhibits the ability of HDAC4 to modify proteins, they found that the mutant mice were able to stay on the rotating rod without falling off – almost as long as the normal mice.

Although the behavioral symptoms and brain cell loss in the engineered mice are not as severe as in humans, all of the biochemical signs of cell stress were reversed and the motor skills improved dramatically in the mice treated with TSA. This outcome proves that brain cell function could be restored, Herrup said.

"The caveat here is that we have fixed a mouse brain with less devastation and fewer problems than seen in a child with A-T disease," said Herrup. "But what this mouse data says is that we can take existing cells that are on their way to death and restore their function."

Neurological degeneration is not the only life-threatening effect associated with this genetic disease. A-T disease – which occurs in an estimated 1 in 40,000 births – causes the immune system to break down and leaves children extremely susceptible to cancers such as leukemia or lymphoma. There is no known cure and most die in their teens or early 20s. According to the AT Children’s Project, many of those who die at a young age might not have been properly diagnosed, which may, in fact, make the disease even more common.

Herrup says although this discovery does not address all of the related medical conditions associated with the disease, saving existing brain cells – even those that are close to death – and restoring life-altering neurological functions would make a tremendous improvement in the lives of these children.

"We can never replace cells that are lost," said Herrup. "But what these mouse studies indicate is that we can take the cells that remain in the brains of these children and make them work better. This could improve the quality of life for these kids by unimaginable amounts."

Additionally, Herrup says, the research might provide insight into other neurodegenerative diseases. “If this is found to be true, then the work we’ve done on this rare disease of childhood may have a much wider application in helping to treat other diseases of the nervous system, even those that affect the elderly, like Alzheimer’s,” he said.

Provided by Rutgers University 

Source: medicalxpress.com

March 30th, 2012

A new animal model of nerve injury has brought to light a critical role of an enzyme called Nmnat in nerve fiber maintenance and neuroprotection. Understanding biological pathways involved in maintaining healthy nerves and clearing away damaged ones may offer scientists targets for drugs to mitigate neurodegenerative diseases such as Huntington’s and Parkinson’s, as well as aid in situations of acute nerve damage, such as spinal cord injury.

University of Pennsylvanian biologists developed the model in the adult fruit fly, Drosophila melanogaster.

“We are using the basic power of the fly to learn about how neurons are damaged in acute injury situations,” said Nancy Bonini, senior author of the research and a professor in the Department of Biology at Penn. “Our work indicates that Nmnat may be key.”

The research was published in Current Biology. First author on the study is postdoctoral researcher Yanshan Fang, with additional contributions from postdoctoral researcher Lorena Soares and research technicians Xiuyin Teng and Melissa Geary, all of Penn’s Department of Biology.

When a nerve suffers an acute injury — as might be caused by a penetrating wound, for example, or a broken bone that damages nearby tissues — the long projection of the nerve cell, called the axon, can become injured and degenerate. The process by which it disintegrates is known as Wallerian or Wallerian-like degeneration and is an active, orderly process.

Though this function of eliminating damaged nerve cells is crucial, biologists do not have a clear understanding of all of the molecular signaling pathways that govern the process.

Bonini’s lab has previously focused on chronic neurodegenerative diseases but made this foray into acute nerve injury to determine if mechanistic overlaps exist between acute axon injury and chronic neurodegeneration. They first searched for an appropriate nerve tract to target and identified the wing of adult flies as a prime option.

The fly wing is not only translucent and a site of lengthy nerve fibers that can be easily observed, but it can also be cut to cause injury without killing the fly. That way, the researchers can follow the animal’s response to nerve injury for weeks.

Using various reagents to manipulate the fly’s genetic traits, the team confirmed that the cut wing nerve underwent Wallerian degeneration. They then tested versions of Nmnat and another protein called Wld^S, all of which had previously been shown to protect nerves from degeneration, to see if any of these might stop the process. All significantly delayed neurodegeneration. Even a form of Nmnat that hadn’t worked in other animal models suppressed degeneration, although to a lesser extent.

“That indicates that our assay is really sensitive,” Bonini said. “This sensitivity could help us identify genes that have moderate although important functionality at protecting against nerve degeneration.”

Their investigations into the wing nerve also showed that the degenerating axon “died back,” fragmenting first from the axon terminals, the side farthest from the nerve cell body—a pattern similar to what has been seen in other disorders.

Doing more genetic tinkering, the researchers showed that when the animal’s own Nmnat was depleted, the nerves fragmented in the same way as if the axon was physically cut. And when Nmnat and the other “rescue” proteins were added back to these genetically modified flies, they were able to block degeneration, highlighting that Nmnat is critical to maintaining healthy axons.

In a final set of experiments, the biologists sought to narrow where in the nerve cells Nmnat might be working. They focused on mitochondria, the powerhouses of cells. When they created a genetic line of flies that blocked mitochondria from entering the axon fibers, the nerve tract degenerated, again, in a dying-back fashion. Yet now Wld^S and Nmnat failed to prevent axon degeneration, suggesting that those proteins may act on and require the presence of axonal mitochondria to maintain healthy nerves in normal flies.

Flipping that scenario around, they looked to see what happened to the mitochondria of flies upon nerve injury. When they cut the wing nerve axons, the mitochondria rapidly disappeared. Yet they can largely preserve the mitochrondria by increasing expression of Nmnat.

Their results, taken together with the findings of other studies, suggest that Nmnat may stabilize mitochondria in some way in order to keep axons in a healthy state.

“We have some hope that these proteins or their activity may someday serve as drug targets or could provide the foundation for a therapeutic advance,” Bonini said. “But right now, my hope is that the power of the fly model will open up a lot of new directions of research and new pathways that could be targets for development in the future.”

Source: Neuroscience News

16:55 30 March 2012

Sumit Paul-Choudhury, editor

My Soul, 2005, Katharine Dowson (Image: Image courtesy of the artist and GV Art)

LOOKING at your own brain is a humbling and slightly unnerving experience. Mine, depicted in a freshly acquired MRI scan, is startlingly intricate, compact - and baffling. This is as much of a portrait of my own mind as I am ever likely to see. But to my ignorant eyes (which, by way of an eerie bonus, are now looking at their own cross-sections) it looks pretty much like any other brain.

Apparently a more expert eye wouldn’t help. “Whilst all my participants get very excited about seeing their brain for the first time after being scanned, and I frequently get asked ‘What can you tell me about my brain?’, the reality is that the brain will for a long time yet remain a mysterious mass,” says the neuroscientist who scanned my brain, for research purposes. “We must be content with knowing that the ‘I’ is constructed in its intricacies, but we cannot explain how.”

The hope of closing the gap between the physical and mental is presumably what gets neuroscientists up in the morning, but it’s frustrating for a layperson like me. Avowed materialist though I am, I nonetheless rebel against the knowledge that the impassive blob on screen is “me”.

This cognitive dissonance was what I took with me to the opening of Brains, a new show at London’s Wellcome Collection, whose subtitle, “The Mind as Matter”, suggests that its curators sympathise with my materialist perspective. “The neurosciences hold out the prospect of an objective account of consciousness - the soul or mind as nothing more than intricately connected flesh,” reads the introduction. But the bulk of the exhibition is dedicated to whole brains, brain collectors and anatomical paraphernalia, with little explicit reference to the brain’s fine structure, or how it might give rise to thought.

This remit is less restrictive than it might sound. Evolution has seen to it that the most vital of our bodily organs is well guarded against intrusion, and as a by-product, well hidden from inspection. Even today, only a small minority of the population have seen their own brains - and many (unlike me, thankfully) have done so only when they had reason to be fearful of what they found.

So the history of attempts to access, visualise and understand the brain is a rich one. But it’s also well worn, and some of the historical material - elaborate anatomical models, kooky phrenological busts and grim-looking surgical implements - is over-familiar. The scientific objects are more compelling, albeit they also tend to the grotesque - from the arachnid contraptions used to measure skull size to the spools of finely-sliced mouse-brains on tape.

Much of the fascination lies not in the objects themselves, but in the human stories behind them, told in captions whose straight-facedness sometimes comes across as drollery or clinical detachment. Trepanning tools fashioned from flint and animal teeth “would have taken longer to cut through the skull than more modern instruments”, one informs us drily; the American Anthropometric Society was “basically a club to enable the leading men of US science to dissect each other,” says another.

Secluded in the skull, individual brains develop relatively few distinguishing features save those given them by trauma, disease or rare accidents of birth. So brains of note tend to be associated with tales of misfortune. That’s often the case with anatomical specimens, but what’s remarkable about the brains on display here is how much they overlap with criminality. Some of the most striking have been acquired from people whose wickedness in life was deemed sufficient reason to deny them dignity in death. In other cases, the moral equation is reversed, with collectors stepping outside the bounds of decency in their desire to possess the brain; the abhorrent nadir being reached with the probable murder of “feeble” children by Nazi doctors.

(Image: Science Museum, London)

The collection’s examples of brains being voluntarily donated are equally remarkable. Persuading someone to donate this most personal of organs is a tough sell, and the historical portion of the exhibition makes much of how appeals to ego have persuaded the great and good to offer up their brains for post-mortem examination. More recently, medical study has provided motivation for would-be donors. Particularly poignant is the tale of Anita Newcomb McGee, a female US army surgeon who gave up her nine-month old son’s brain, along with a photograph and a sketch of his head, with the words “I want him to benefit the world in some way if possible.”

But this altruism is tempered by the fact that brains, unlike many of our other “charismatic organs”, cannot conceivably be transplanted. The knowledge that someone else might gain life from my gifted heart is a powerful incentive to donate, but I have less incentive to be generous with my brain - though it would seem that distinction is not made by those who do donate. Perhaps reluctant donors might be won over by the moving photos compiled by artist Ania Dabrowska and social scientist Bronwyn Parry of cheerful would-be donors ranging from an ex-soldier to a headmistress.

And one of the exhibition’s stand-out exhibits might provide further reassurance: a documentary video of anatomists at London’s Hammersmith Hospital painstakingly and precisely slicing donated brains into half-centimetre wedges in near-silence. Or perhaps not. This is well sanctioned, respectful science being conducted on freely donated organs for the betterment of human health and knowledge; and yet it nonetheless provokes one of my fellow spectators into muttering, very much to herself: “Wrong, wrong, wrong”. For myself, I find the video one of the most compelling exhibits — perhaps the only one that prompts me to contemplate offering myself up for more than a non-invasive scan in the service of medical science.

Less clear-cut, for me, are the nearby sections of Einstein’s brain, preserved under deeply dubious circumstances after his death. Clearly, there’s a certain fascination associated with perhaps the most famous brain there ever was; but Einstein’s brain is no more legible than any other, and the slim prospect that scientific insights can be gleaned from its study seems poor recompense for the undignified proxying of a great mind by illicitly-obtained fragments of tissue.

(Image: Wellcome Library, London. Wellcome Images)

The final insult: an accompanying 3D-printed replica of the entire organ, reconstructed for a TV documentary from archive photographs. This absurd resin relic epitomises, for me, the extent to which the objects on display at the Wellcome are imbued with significance by the knowledge that they were once the seats of consciousness. It’s the minds of the audience, rather than the brains on display, that are doing the work.

The Wellcome show confronts its visitors with the gulf between our hard-won knowledge about the form of the brain and our as-yet-meagre understanding of its function, much as my scan did to me. It didn’t narrow the gap between the grey image of my brain and my sense of self; if anything, it widened it. But it did make me appreciate what an amazing gap it is, and marvel anew at the work of those who are seeking to close it.

Brains: The mind as matter is showing at the Wellcome Collection in London until 17 June.

Source: New Scientist

March 30, 2012

A team of neuroscientists from the Institute of Psychiatry (IoP) at King’s College London have developed a digital atlas of the human brain for iPad. The ‘Brain’ App is the first of its kind, and is based on cutting edge neuro-imaging research from the NatBrainLab at the IoP. 

Image taken from the ‘Brain’ Study Room

Dr. Marco Catani, Head of the NatBrainLab who led the development of the App with Dr. Flavio Dell’Acqua and Dr. Michel Thiebaut de Schotten, said: “For 10 years our lab has pioneered the use of highly advanced neuro-imaging techniques. This is the first time that imaging methods usually only applied to research have been used in an educational App. It’s very exciting to see our work transformed into such an accessible, fun and beautiful tool.”

Image taken from the ‘Brain’ Dissection Room

Two types of scans were used to develop the content of ‘Brain’ – results from an MRI scan reveal the structural properties of the brain, and images from a Diffusion Tractography scan allow the user to identify connections in the brain. 

The App is split into two virtual rooms. The Dissection Room allows the user to play with a 3D human brain, select individual structures and ‘pull’ them apart to visualize their anatomical features. The Study Room then offers a more thorough explanation of functional aspects and their relationship to neurological and psychiatric disorders. 

Dr. Catani adds: “The interactive nature of our App really allows you to explore the depths of the neural network and appreciate the complexity of the human brain. Because the content is based directly on research, the finished product is an accurate reflection of the real thing.”

Dr. Catani and his team are now working towards developing the next version of the App. By integrating scans from several different brains into the programme, they hope to be able to offer the user the chance to see directly how the brain develops from childhood to old age and the direct effect of different age-related disorders on the brain.

The App is currently being used by Dr. Catani and his colleagues to teach MSc students neuroscience.

Provided by King’s College London

Source: medicalxpress.com