At his State of the Union address nearly two months ago, President Obama announced plans for the Brain Activity Map (BAM) project (see The Nerve blog Part 1 and Part 2), a billion-dollar ten-year research initiative to gain a better understanding of the brain and to provide deeper insights into diseases like Alzheimer Disease, Parkinson Disease, and Autism Spectrum Disorder.

On Tuesday, April 2^nd, the President announced that he plans to include the BAM project – now termed the BRAIN (Brain Research through Advancing Innovative Neurotechnologies) Initiative – in his 2014 budget proposal. The director of the NIH, Dr. Francis Collins, notes that one of the major goals of the project is to simultaneously sample from many neurons in real-time. Although existing technology can measure the activities of single neurons and of brain regions, it cannot measure those of circuits. Because existing technology has not yet advanced to a level that allows such complex analysis, the BRAIN initiative will be initially funded $100 million for the year of 2014 to develop and advance neuroscience technologies. Yearly negotiations will take place to determine future funding.

Over the next several months, 14 leading neuroscientists from Stanford, CIT, Harvard, Brown, Princeton, and Brandeis will serve on the advisory board (also called the “dream team” or the “brain trust”) to refine the project’s immediate and long-term goals. They will need to decide which research areas are of high priority, which projects require more funding, and which technologies need to be developed and employed. Additionally, President Obama has required a study to explore the ethical, societal, and legal problems associated with the project’s advances in neuroscience.

Dr. Francis Collins and President Obama on Tuesday, April 4th at the White House

Although $100 million may not be sufficient to transform neuroscience, it may “help get this project off the ground,” as President Obama says, and forge a new path for advancing neuroscience. In fact, Francis Collins notes that the Human Genome project was only funded $28 million for its first year. Further, private organizations including the Allen Institute for Brain Science, the Salk Institute for Biological Studies, the Howard Hughes Medical Institute, and the Kavli Foundation have already committed $158 million.

Just as genetics research had been underway before the Human Genome Project, neuroscience research has been going on long before the announcement of the BAM project or the BRAIN initiative. Hopefully, this investment in neuroscience research will do for neuroscience the same that the Human Genome Project did for genetics: provide a plan considering the state of current research, speed up the process of improving the state of knowledge, bring more money into the economy than funded, recruit additional experts to foster an interdisciplinary effort, and capture the interest of the general public. The BRAIN Initiative should provide a goal-oriented long-term focus and allow the coordination and collaboration of neuroscientists in advancing biology, health, medicine, and society.

“Of course, none of this will be easy. If it was, we would already know everything there was about how the brain works, and presumably my life would be simpler here. It could explain all kinds of things that go on in Washington.” – President Obama

-Margaret McGuinness

Sources:

Eve Marder joins Obama neuroscience ‘brain trust’ – BrandeisNOW

Obama outlines private-public project to study the brain – Los Angeles Times

Neuroscience: Making connections – Nature

Obama to Unveil Initiative to Map the Human Brain – New York Times

BRAIN Initiative – NIH

A Brief History of the Human Genome Project – NIH NHGRI

Researchers Question Obama’s Motives for Brain Initiative – NPR: Morning Edition

President Obama Calls For A ‘BRAIN Initiative’ – NPR: Talk of the Nation

BRAIN Initiative Challenges Researchers to Unlock Mysteries of Human Mind – The White House Blog

Fact Sheet: BRAIN Initiative – The White House: Statements and Releases

…Says the slime mold before the zombie ate its brain centuries ago, forcing the whole species to adapt into its present state: brainless yet smart.

Slime molds avoid bright light. In A, there was none, so molds grew to food (yellow puncta) freely while in B and C there were differing shades of light to influence its growth, which is surprisingly comparable to the real Tokyo rail network in D. E and F show minimum spanning trees (see third source below).

Okay, the zombie part isn’t entirely accurate, BUT, these slime molds (the gelatinous amoebae also known as the protist, Physarum polycephalum) do seem to have no problem functioning without a brain. They can navigate complex mazes for food, choose healthy over less nutritious food, and determine the shortest route between points of interest – a feat that takes humans years when designing complex transportation systems. How could this be?

Scientists have been studying this protist for over thirty years, taking it to the lab from its natural environment, where it has searched for food in leaf litter and along tree limbs to envelop and digest for at least 600 million years (essentially, dumpster diving before it was cool). Following studies in the early 2000s by Toshiyuki Nakagaki at Hokkaido University in Japan, Chris Reid at the University of Sydney observed that slime molds avoid spots they have traveled on, which was thought to demonstrate an externalized spatial memory that encourages exploration. Additionally, when placing the molds in a dish with dry acetate blocking access to food, Reid observed that molds navigated around the obstacle to the food. However, when he added extracellular slime prior to placing the molds in the dish, he noted that the molds had significantly less success finding the food, demonstrating they were “confused” and could no longer map areas traveled.

Time lapse of slime mold starting at "Tokyo" in an experimental arena and creating a network between major cities in white marked by pieces of food (third source below).

Other studies how shown how slime molds can choose optimal travel routes and foods. As a pretty good “shape-shifter,” flattening, thinning, and accumulating as needed, slime molds have been seen to leave areas that are dead-ends in mazes in favor of areas that lead to food. Slime molds similarly left or thinned out in areas that were less optimal, leaving behind interconnected routes that resembled rail-lines and main roads in places like Tokyo. Although the protists may not get paid for their unexpected proficiency in navigation, they may be used in the planning of future transportation routes or to create computer models simulating their decision-making processes, suggests some researchers.

Slime molds not only navigate surprisingly well, they have also been suggested to have internal clocks. Tetsu Saigusa, also at Hokkaido University, found that these internal clocks may allow slime molds to anticipate events by monitoring the rhythmic pulsing of their cytoplasm (also responsible for flowing from one region to another though periodic constrictions and relaxations). When subjected to unfavorable conditions periodically, slime molds slowed their cytoplasmic pulsing. For some slime molds, this slowing trend continued even when exposed to consistently favorable conditions. Eventually, even those molds ceased the slowing of their pulsing, enjoying the good life of humidity and high temperatures.

And apparently, a good life means good food too. Slime molds have been shown to choose the best balance between carbohydrates and proteins when placed near one protein-rich food and one carbohydrate-rich food through adjusting their size. In one study, Dr. Beekman at the University of Sydney placed 3% and 5% oat flakes under bright lights, which slime molds try to avoid (despite liking heat and humidity). The slime molds traveled from dark to light areas for the oat flakes but without a preference of percentage. However, when 1% oat flakes were placed in the dark, they went to the 1% oat flake, suggesting that, like humans, slime molds choose based on relative, not absolute, values, deciding based on priorities.

Certainly, slime molds seem to be prioritizing and optimizing their behaviors. Scientists have been trying to sequence the DNA of the many species of slime molds to explore how they have evolved, and to elucidate what allows the organism to retain memories and optimize decisions.

The question then remains, are these protists an “intelligent” species? As a human and a neuroscience major, I have been taught the importance of centralized nervous systems to intelligence. Then this slime mold comes along, leaving behind externalized memory traces and optimizing its decisions lacking anything even close to a brain. Where’s its hippocampus? Does it not have a dentate gyrus? Where are the granule cells? Neuroscientists, biologists, scientists, psychologists, and so on must then wonder, what makes an organism intelligent? What are the anatomical and functional criteria? One thing is certain,  these slimy protists are challenging our understanding of intelligence, one disgusting, oat flake-coated petri dish at a time.

Sources:

Physarum Music – YouTube

How Brainless Slime Molds Redefine Intelligence [Video] – Scientific American

Rules for Biologically Inspired Adaptive Network Design – Science

Can Answers to Evolution Be Found in Slime? – The New York Times

The gastrointestinal (GI) tract in humans provides a home for many (10¹⁴) bacterial organisms. The colonization of the GI by bacteria, or microbiota, starts at birth and continues throughout early development and life. These microbiota affect many bodily functions, aiding metabolism, modulating inflammation, and defending against harmful micro-organisms. Each person has a unique profile of microbiota, which is influenced by genetics and the environment. Healthy people, however, generally have similar numbers and distributions of microbiota. Interestingly, disorders of the GI tract have a high comorbidity with mental illness.

It is not surprising then that research in this field has grown, with labs hoping to gain a better understanding of the ‘gut-brain-axis.’ If these labs can elucidate the effect of microbes in the GI tract on the central nervous system, they could shed light on why more than half of patients with irritable bowel syndrome meet the criteria for mood disorders, or how GI tract disorders and mental illnesses can be more effectively treated.

Many researchers are currently focusing on how variations in the composition of microbiota impact physiology and contribute to disease, such as obesity and inflammation. Increasingly, studies have been revealing that these microbiota communicate with the brain and influence its function and behavior, potentially by neural, endocrine, and immune pathways.

In 2010, Jane Foster and colleagues at McMaster University in Ontario found that microbiota may affect gene activity during central nervous system development. They compared how germ-free and normal mice act on an

Elevated plus maze used for testing anxiety-like behaviors in mice (from the Mouse Phemone Database)

elevated plus maze (shown to the right) that is used for testing anxious behaviors. Normally, mice avoid areas they might be seen and spend more time in the less visible arms of the maze.

While the normal, control mice did spend more time in the ‘closed’ over ‘open’ arms, germ-free mice spent more time in the open arms, exploring them and showing less anxious behaviors. After the experiment, Foster and her team examined the brains of the mice and found alterations in the gene expression levels of several genes in the germ-free mice, particularly in those affecting brain-derived neurotrophic factor (BDNF) and serotonin (5HT). BDNF and 5HT had been previously suggested to affect emotion and anxiety.

Importantly, the study shows that the absence of microbiota can alter behavior and suggests that the microbiota in the GI may impact gene expression during the sensitive period of early brain development. Although studies in mice need to be proven translatable to humans, a pediatrician was interested in collaborating with Foster to determine if he could determine a way to fix the microbiota profile of some of his patients before puberty.

Using germ-free animals and animals exposed to infections, researchers have suggested a role for microbiata in regulating mood, anxiety, cognition, and pain. More research is needed to decide whether formulating or modifying gut microbiota could serve as a possible therapeutic for central nervous system disorders. Foster suggests combining preclinical work on microbiota with clinical work on the impact of antibiotics and probiotics on brain development and function. This could allow researchers to better understand bottom-up control and provide inspiration for novel interventions in mental illness. In the end, communication between scientists and clinicians in various fields and domains is crucial to determine the relationship between gut microbiota and the central nervous system.

Sources:

Microbes Manipulate Your Mind – The Guardian

Mind-altering microorganisms: the impact of the gut microbiota on brain and behaviour – Nature Reviews Neuroscience

Effects of gut microbiota on the brain: implications for psychiatry – Journal of Psychiatry and Neuroscience

Reduced anxiety-like behavior and central neurochemical change in germ-free mice – Neurogastroenterology and Moltility

Know any of the above words from ubongo to brein? If so, you can (surprisingly to you of course) say BRAIN in Hawaiian, Swahili, Spanish, Italian, French, or Dutch. And if you can (read this and) fluently speak at least one of these languages, or another not shown, you are multilingual (again, SO surprisingly to you…) – and may consequently reap some benefits from this status!

According to the U.S. Census Bureau, at least 13% of Americans are bilingual. They speak a language other than English at home and can speak English “well” or “very well.” Henceforth, studies on bilingualism are relevant and many have actually demonstrated differences between monolinguals and bilinguals.

Despite political adversity, educational neuroscientists have advocated the study of second languages in school and the use of a second language at home, especially before age five or six. According to a briefing from the Society for Neuroscience website, monolingual and bilingual children have been found to reach the language milestones at the same time and the latter are not “language confused” as some adversaries and earlier theories would suggest.

Several studies have demonstrated that bilinguals perform better than monolinguals on many executive control tasks, including attention, control, concentration, inhibition, and prioritizing. In the Los Angeles Times, Ellen Bialystok from York University in Toronto who has studied bilingualism for nearly 40 years discussed a study in which she found that bilinguals “manifested a cognitive system with the ability to attend to important information and ignore the less important.” Compared to monolingual children, bilingual children would pick out silly sentences like “apples grow on noses” but also note that they are still grammatically correct.

Additionally, bilingual people were found to “multitask better, pick out key information faster and more effectively ignore surrounding distractions.” In the Stroop test, where one must say the color of the letters rather than the word made up from the letters (e.g. the word blue written in red), bilingual people had faster reaction times than monolingual people – 160 milliseconds compared to 240 milliseconds.

Another study by Krizman et al. in 2011 noted that bilinguals showed “enhanced discrimination of simple, non-linguistic sounds as assessed by a measure of temporal resolution (backward masking) and a measure of frequency discrimination.” Supposedly, bilingual brains can better process “specific sound elements that relate to auditory perception and cognitive abilities.”

Such enhancement of cognitive abilities has been suggested to protect bilingual people from the symptoms of dementia and Alzheimer Disease. According to the Society for Neuroscience website, some theories suggest that “speaking two languages may increase blood and oxygen flow to the brain and keep nerve connections healthy—factors thought to help ward off dementia.”

Another study by Bialystok from 2004 showed that bilingual people had enhanced cognitive function compared to monolingual people. Later studies looking at the medical records of around 400 patients demonstrated that bilinguals also showed Alzheimer Disease symptoms five or six years later than monolinguals.

While learning a language could protect us from showing symptoms of Alzheimer disease, performing any kind of engaging task that requires more than one sensory modality can help. In doing so, the brain strengthens neural networks and could rewire in some areas. According to Bialystok, bilingualism does rewire the brain. Neural connections are different between monolinguals and bilinguals. Neuroimaging demonstrates that, when solving a problem or performing a task, different systems are being used by the two groups. Additionally, another study showed that the inferior parietal cortices of bilinguals have greater gray-matter density in the language-dominant left hemisphere, especially in those who were proficient early on in life. Not only that, but the dorso-lateral prefrontal cortex of the right hemisphere is more active when bilinguals are “toggling” between languages, or in “bilingual mode.” This area has been known to take part in attention and control, and its activity acts as a neural signature of bilingualism.

While more studies are needed to challenge theories, many have persuasively shown that there is a difference between bilinguals and monolinguals, and this difference provides bilinguals an advantage in executive control and prevention of cognitive decline.

What language will you try to pick up?

Sources:

Brain Briefings – Bilingual Brain, Society for Neuroscience

Bilingualism good for the brain, researchers say - Amina Khan, Los Angeles Times

J.L. Krizman Presentation Abstract

The Bilingual Advantage – Claudia Dreifus, The New York Times

According to a recent study, there are at least two neural correlates for decision-making in the brain.

If you’re the scarecrow in the Wizard of Oz who yearns for a brain, you have neither of these correlates. However, if you are someone who has frontal lobe damage to the orbitofrontal cortex (OFC), you have one functional neural correlate: for action value comparisons. You can make optimal decisions about how to get a brain (…although you obviously would already have one). Alternatively, you could have suffered damage to the dorsal anterior cingulate cortex (dACC) - in which case you would be able to make stimulus value comparisons and choose which objects are optimal, such as the wittiest or the most creative brain, but not how to get the chosen object.

These findings on stimulus and action value comparisons came from the study conducted by Camille et al. at McGill University. The authors tested human subjects with frontal lobe damage to either the OFC or dACC compared to controls. The behavioral tests were computerized value-driven learning tasks that were given on two different occasions. By comparing the overlap of lesions from the brain scans of patients, they suggested that damage in certain areas either altered stimulus or action value comparisons, both of which have been known to be important in the decision-making process.

Dr. Lesley Fellows, a neurologist and research scientist at The Neuro – or the Montréal Neurological Institute and Hospital, was the principal investigator. She says, “The surprising and novel finding is that in fact these two mechanisms of choice are independent of one another. There are distinct processes in the brain by which value information guides decisions, depending on whether the choice is between objects or between actions… This finding gives me more insight into what is happening in the brain of my patients, and may lead to new treatments and new ways to care for them and manage their symptoms.”

Certainly understanding more about the decision-making process in terms of the neural correlates is important in creating and deciding on treatments for patients, as well as providing more information, coping strategies, therapy, and better care to those who suffer brain damage affecting their decision-making abilities. Not only that, but this understanding also provides a clearer perspective on frontal lobe dysfunction and other disorders that may include symptoms like indecision or risky behavior.

Decision-Making: What You Want Vs. How You Get It – Science Daily

Double Dissociation of Stimulus-Value and Action-Value Learning in Humans With Orbitofrontal or Anterior Cingulate Cortex Damage – Nathalie Camille et al.

Lobsters, Axons, Telephones, and Extracellular Recordings – A look at how neuronal signals can be transmitted differently under certain pharmacological conditions.

Neuronal signals are normally transmitted from cell bodies, or somas, to terminals via extensions called axons. At these terminals, connections called synapses are made with other neurons whereby the signals are released via the aide of chemical messengers called neurotransmitters. Many still believe that axons are reliable conductors of these signals.

However, with several years’ worth of experiments, scientists have questioned the fidelity of axonal conduction. They’ve realized that axons do not work like telephones. While telephones and axons may both have buttons – at the terminals in axons – only telephones faithfully conduct signals. And only telephones ring aloud and send messages to voicemail…

In any case, neuronal signals, unlike telephone signals, can change along their paths. Moreover, the pre-synaptic neuron may communicate a different message from the one originally sent from the soma to the synapse with the post-synaptic cell.  Researchers at the lab I’ve been working at this summer, the Whitney Laboratory for Marine Bioscience, have focused on the role of neuromodulation in signal transmission along axons, particularly by the well-known neurotransmitter – dopamine.

Top Left, Homarus americanus. Bottom Left, Nervous system pinned down for recordings. Right, Recordings in vivo and in vitro.

Dissecting out the stomatogastric nervous system of the Homarus americanus, or Maine Lobster, Dirk Bucher, Aleksander Ballo, and colleagues have been able to take extracellular – and intracellular – recordings from axons. Using these recordings, they focus on how signal transmission differs under control and pharmacologically affected conditions.

Bucher and Ballo are some of the first researchers to directly show that neuromodulators affect activation properties of axonal voltage-gated ion channels – particularly looking at HCN channels. First off, these channels carry the hyperpolarization-activated inward current, which brings positive ions into the axon and initiates depolarization. Secondly, researchers including Ballo and Bucher suggest these channels influence neuronal communication by affecting the timing and efficacy of spikes and bursts. Further, they suggest the channels balance positive and negative currents to improve fidelity when there is repetitive spiking; this type of spiking can occur through many central pattern generators, such as those involved in rhythmic behaviors like walking, chewing, and swimming.

Spikes can also be initiated peripherally by dopamine administration. Ballo and Bucher offer that dopamine acts through D1-type receptors to increase cAMP which then works to modulate HCN channels.

Second messenger mechanism by which dopamine increases cAMP to influence HCN channels and corresponding currents

Often this series of events increases axonal conductance. When the current at these HCN channels is blocked, dopamine has no effect, suggesting also its importance in fidelity of axonal conduction.

Hopefully with more research into how signals can be altered after production at the soma, we can better understand how rhythmic behaviors are initiated, maintained, and restored.

Source: Dopamine Modulates I_H in a Motor Axon – Ballo, Bucher, et. al, The Journal of Neuroscience

With the Pancakes for Parkinson’s event at Boston University nearing, on April 2^nd, I thought it would be a good time to check up on the latest in Parkinson’s research.

Firstly, Parkinson’s Disease (PD) is a motor disorder that affects dopaminergic neurons of the brain, which are necessary in the coordination of movement. Onset is usually around age 60, starting with symptoms including tremor, stiffness, slowness of movement, and poor balance and coordination. While current treatments can help alleviate the symptoms in patients, none provide a cure.

Second off, the mission of the Michael J. Fox Foundation for Parkinson’s Research and other support groups is to find better treatments for those suffering from the disease. With the Baby Boomer generation entering late adulthood and old age, more research needs to be done to better understand the disease and help those with it find relief. Consider stopping by the GSU Alley for some pancakes to show your support for the Foundation and its cause next month!

Ranging from studying food intake to using technology, many approaches have been used in PD research.

FOOD

In a study released in February from the Harvard school of Public Health, flavonoids (citrin and Vitamin P), found in chocolates, citrus fruits, berries, and other foods, were speculated to reduce the risk of Parkinson’s Disease (PD).

The top 20% of males consuming these foods were 40% less likely to develop PD than the bottom 20%. While the overall flavonoid intake had no effect on women, a subclass of flavonoids called anthocyanins, which are primarily found in berries, did.

Study author Dr. Xiang Gao notes that this subclass has neuroprotective effects. Dr. Carlos Singer of UMiami’s Miller School of Medicine adds that the risk reduction “probably has to do with an antioxidant effect” because a lot of PD mechanisms deal with how nervous tissue handles oxidative stress.

Dr. Anna Hohler, a neurologist and professor at our very own, Boston University, was not involved in the study, but she comments on its benefits, saying that it “opens up a whole area of potential future studies examining other types of environmental effects on Parkinson’s.”

Hopefully, with more research we can determine whether these berries play a role in risk reduction. For now, Gao encourages us to eat berries anyway – they’re part of the reason why fruits and vegetables are so good for our health! Want to start a regular berry-eating habit? BU’s Mind and Brain Society is actually hosting another Miracle Berry event March 23^rd. Soon enough, you can reap the benefits of berries, AND have a taste-altering experience – find out how bitter foods can taste quite sweet when these berries intervene then!

DRUGS

Berries are not the only things that affect PD. Drugs, of course, do. One drug is the psychostimulant – amphetamine. According to a study released in February, amphetamines may increase the risk of PD, in contrast to the berries. Researchers found that those using the amphetamines Benzedrine or Dexedrine at some point in their lives were 60% more likely to develop PD compared to those who never used. Why? According to the report, amphetamines affect the release and absorption of dopamine, a neurotransmitter associated with PD development. More on the mechanisms causing this difference still need attention.

Another drug to consider is apomorphine, which is used to alleviate PD patients’ motor symptoms. Amazingly, this drug has also been found to improve short-term memory in mice with Alzheimer’s Disease, which, like PD, affects brain function. According to a study released in October, 2010 by Japanese researchers at Kyushu University, the drug reduced the levels of amyloid beta, a protein that reduces brain cell function; it led mice to improve their times in a swimming test conducted before and after the drug was injected.

The results, indicating improved memory function, “will lead to the development of a new treatment for Alzheimer’s disease,” says Associate Professor Yasumasa Oyagi. His group plans to perform clinical testing on human patients to develop a drug with few or no side effects (apomorphine can cause nausea and vomiting).

While not directly influencing PD patients, this development is inspiring; perhaps drugs used to treat other neurodegenerative diseases can help treat PD as well.

PROTEINS

In their study published March 4^th, Researchers at John Hopkins found that, when the parkin gene is mutated in genetically altered mice, the protein PARIS accumulates since its degradation is blocked. Excess decreases the production of PGC-1alpha, a protein that protects brain cells, such that unprotected cells die and PD advances.

“Of all the important changes that lead to the death of brain cells as a result of parkin inactivation, our studies show that PARIS is, without a doubt, a key player,” says Ted Dawson, M.D., Ph.D., of the Johns Hopkins Institute for Cell Engineering.

STEM CELLS

A press release March 3^rd announced that Stanford researchers used induced pluripotent stem cells to model PD. With the skin of a woman with a genetic form of PD, they derived neurons that replicated “some key features of the condition in a dish.” They hope to test treatments on and learn more about PD from these neurons.

TECHNOLOGY

A study published in September, 2010, demonstrates an approach to PD treatment through technology, specifically virtual reality. Researchers involved wanted to reduce “fall risk and difficulties with mobility, especially during complex or dual-task walking.”

Using virtual reality, they can better “incorporate principles of motor learning while delivering engaging and challenging training in complex environments.” At the end of the training, they observed a significant improvement in gait speed, particularly in walking, dual task, and facing overground obstacles. One month after the training, researchers still observed these effects. The group hopes to continue research on motor learning and fall risk reduction.

PSYCHOLOGY

From a review published in January, neuroscientists examined studies on Theory of Mind (ToM), “the ability to infer other people’s mental states,” in those with PD. They found “preliminary evidence that ToM difficulties may occur in PD patients,” particularly in the “cognitive component of ToM in the early stages of the disease.”

SOCIETY

Paul Green of Westport, CT was diagnosed with PD 17 years ago. Since then, he has searched for ways to slow its progression, finding some that have allowed him to live into his 80s. Now 87, he denies that symptoms like depression and tremor will occur.

Compiling his research, he wrote a booklet on his conclusion that progression can be slowed with “vigorous exercise.” Using this and his foundation Nevah Surrendah to Parkinson’s (inspired by Winston Churchill’s use of “nevah” in WWII), he aims to help others with PD.

He believes that with “prescription drugs, deliberate exercise and changes in nutrition and attitude they can enjoy a full life.” He continues, “What works for one person might not be as helpful for another. However, it’s vital that people ‘nevah’ stop trying to improve their physical, spiritual and emotional condition.”

Whether people eat more berries, exercise more, or cut down on amphetamines, they are making attempts to fight PD. Thanks to the research using so many different approaches, a lot has been discovered about the disease. However, it is quite clear that many more studies need to be carried out to affirm the conclusions above and better understand the mechanisms of PD. For now, with awareness and support of Parkinson’s Disease research, the goal is to find the best treatments for patients and most earnestly a cure.

Sources: Berries may offer sweet protection against Parkinson’s — Steven Reinberg of The Jackson Sun; Certain foods could reduce risk of Parkinson’s? Berry possible. – Tyler Moss of Northwest Indiana (NWI) Times; Parkinson’s drug ‘helped mice with Alzheimer’s’ – The Daily Yomiuri; Can Prescription Amphetamine Use Raise Parkinson’s Risk? – Stacy Lipson of Bloomberg Newsweek; Johns Hopkins Team Explores Paris; Finds A Key To Parkinson’s – Press release by Maryalice Yakutchik; Stanford scientists create neurons with symptoms of Parkinson’s disease from patient’s skin cells – Press release by Krista Conger; Virtual Reality for Gait Training: Can It Induce Motor Learning to Enhance Complex Walking and Reduce Fall Risk in Patients With Parkinson’s Disease? – Anat Mirelman, et al. from the Journals of Gerontology; Theory of Mind in Parkinson’s disease – Michele Poletti et al. from ScienceDirect; Westport man refuses to surrender to Parkinson’s – Karen Kovacs Dydzuhn of Westport News

Zombies attack! – well, the media, anyway. From movies and television shows (this past Sunday on Glee!) to books and conventions, zombies are taking over. Last year, “Seattle, the self-proclaimed zombie capital of the world, was host to ZomBcon, the first ever Zombie Culture Convention, over Halloween weekend at the Seattle Center Exhibition Hall.

A “symbolic tribute” to zombie film director, George A. Romero, the event allowed fans to gather over three days to “celebrate all things zombie.”  The creator, Ryan Reiter, also organized a Red, White & Dead Zombie Walk for Independence Day (Guinness Book World Record for “largest gathering of zombies” with 4200… New BU Initiative: Beat this Guinness Book World Record?)

Back to zombies though – on April 13^th, 2009, Dr. Steven Schlozman , a Harvard psychiatrist, went to the Coolidge Corner Theater (close by in Brookline!) to discuss and answer questions about the neurobiology of zombies before a screening of Night of the Living Dead.

Having studied zombie films and literature as well as consulting with the director Romero noted above, Dr. Scholzman is quite informed in zombie-ology. Amazingly, the enthusiastic response from the moviegoers inspired him to go viral and, according to Rebecca Jacobson on PBS, “take the lecture nationwide.”

Ira Flatow of National Public Radio had an interview with him in October 2009, in which of Dr. Scholzman, he says his fake research aids attempts to “see if there could be…a vaccine to protect us from … zombies, just in case.” Later, when asked by a caller about the different kinds of zombies portrayed in movies, he distinguished between the typical, slow Romero-type of zombie and the fast, more sophisticated “28 Days later” type that can exhibit hunting and other pack behaviors – “neurobiologically speaking, they got to be different.”

He has actually also written a popular science book, The Zombie Autopsies: Secret Notebooks from the Apocalypse. With 208 pages of zombie-brain-apocalyptic fun, his book will be released March 25^th, 2011 for as little as $11.25 on Amazon. (Check out his zombieautopsies twitter for more on the book and his theories!)

Rebecca Jacobson notes that Dr. Scholzman is using a very straightforward, fun, teaching approach to help his students apply neuroscience to new situations. Dr. Scholzman believes adults “learn better when they can apply new knowledge to something familiar, before going on to tackle more complex neuropsychiatric cases.”

Teaching science in new ways is very valuable to Doron Weber of the Sloan Foundation, which has “has promoted filmmakers writing screenplays and making movies with science themes.” He says, “science and technology are woven into the fabric of our lives, but people all too often see it as something exotic or unusual. What we are doing here is bringing the real person, a scientist, so people can see that science is a very human activity.”

The Coolidge Corner Theater tries to bring science to the public by holding Science on Screen events, tickets only $7.75 for students. This February 21^st, the film Death in Venice will be screened following a discussion with Nancy Etcoff, who is a psychologist on the faculty at Harvard Medical School. She wrote Survival of the Prettiest: The Science of Beauty. Just a month later, on March 21^st, Transcendent Man will be screened and discussed with both Ray Kurzweil, “one of the world’s leading futurists,” and director Barry Ptolemy. Go to http://www.coolidge.org/science for more information!

Back to brains though! In Dr. Scholzman’s fictional, futuristic papers on the neurobiology of zombies, he writes that zombies suffer from ANSDS (Ataxic Neurodegenerative Satiety Deficiency Syndrome). He strives to explain the hunger, rage, movement, and so forth of zombies. Interestingly, he says that zombies can only be fueled by rage, like crocodiles, and hence, have highly active amygdalae. Because of this, he originally named their syndrome RAH (Reptilian Aggression Hunger Syndrome), but that was before the fictional International Classification of Disease decided to change it to ANSDS in “2012”… find out more, including his theory on how zombies always eat but never..you know excrete, here!

While Dr. Scholzman is not the only person to try to explain the neuroscience of zombies, he does it very well and has been received enthusiastically by many. Interestingly though, the new hit TV series, The Walking Dead, attempts describing what happens to the brain after infection and into resurrection. Watch this Youtube clip to see Dr. Edwin Jenner use MRI virtual camera to show the other characters what he has learned of zombies! How does his explanation line up with Dr. Scholzman’s? What’s your theory?

Sources:

A Head-Shrinker Studies The Zombie Brain – Ira Flatow, National Public Radio

ZomBcon 2010: Seattle Hosts First Ever Zombie Convention – Timothy Lemke, Yahoo! Games, Plugged in

A Harvard Psychiatrist Explains Zombie Neurobiology – Mark Strauss,  io9 forum

What Zombies Can Teach Us About Brains – Rebecca Jacobson, PBS

Silver Screen Scientists Unleashed – Dan Vergano, USA Today

Imagine that you’ve just spent the whole morning working non-stop. You’ve been hushing your stomach grumblings for the past hour and you cannot concentrate on anything but your hunger and that devastatingly slow-ticking clock.

Another hour passes and that long awaited lunchtime break has finally come around. All you know is that you need food, and you need it now, so you decide to stay in your building and rush to the cafeteria. You enter, put your things down, and begin the search.

Which foods will you choose? Or, which foods will choose you?

Brian Wansink and David R. Just are trying to answer that question, specifically pertaining to children. In addition to being faculty at the Dyson School of Applied Economics and Management at Cornell, Wansink and Just are co-directors of the newly launched Cornell Center for Behavioral Economics in Child Nutrition Programs. With a $1 million grant from the U.S. Department of Agriculture, the center will provide valuable research on subtle behavioral influences, helping efforts to “nudge” children into making healthier eating choices.

Wansink says, “We’re taking some of the best researchers in the nation and pairing them with schools to figure out new, cool ways to get people to eat healthier.” For example, “by strategically placing healthy food at both the beginning and end of school lunch lines, more children choose them.”

Naming foods more descriptively, charging extra for dessert, and placing healthy foods like fruits into baskets also increased choice of healthier foods. Other interesting techniques Wansink and Just suggest can be seen in Joe McKendry’s illustration in The New York Times.

The benefits of this research seem clear enough. Children who are encouraged to eat healthier each day at school will likely develop long-lasting, healthy habits. These habits can then help reduce their risk of obesity and associated diseases.

So what about the drawbacks? Are there any? Is changing the way options are presented a violation of free will or choice? Just says he and his colleagues are “not eliminating choice… [they’re] pushing things where [they] can and not trying to do the impossible.”

What do you think? Are there degrees of choice? Are Just and Wansink simply lowering the degree children have in selecting foods to eat? Either way, isn’t it sort of disturbing that such subtle changes in placement, naming, or presentation can influence your decisions, whether it be which foods you eat or which habits you’ll develop?

The research in the rising field of behavioral economics certainly leads one to ask these questions. Author of Predictably Irrational, Dan Ariely talks on TED about how irrational people are in their decisions. Particularly, he discusses how easily external forces can influence choices. For example, depending on how a question is worded or presented, people respond differently even though the two forms of the question are essentially the same.

One interesting study he conducted involves choosing the image of the most attractive man out of a total of three men. Two of these images are of the same man, Jerry, but one is edited to make him less attractive by distorting the facial features. The other image is of another man, Tom. Most participants chose the more attractive version of Jerry. However, if instead there are two images of Tom, one less attractive, and one image of Jerry, most people choose the more attractive version of Tom. Even though the original images of Tom and Jerry remained in both sets, they did not receive the same response because of an external force.

Through these examples, Ariely demonstrates how much influence the designer, whether of surveys, forms, or tests, has on the decisions of the people filling them out. Do the people still have a choice to choose Jerry when unattractive Tom highlights regular Tom so well? If yes, then why do most people choose Tom? Are there degrees of choice involved? How about degrees of resistance to external forces? Do they change at all when the designers have different intentions? For example, compare a store selling 2 shirts for the price of one and a cafeteria offering “creamy corn” and “two-dollar cookies.” Both places are trying to take advantage of subtle differences, but the cafeteria seems to have kinder intentions.

What can we make of all this? Can we change how irrational, as Ariely might say, we are? If so, should we advocate the advances of behavioral economics in their kinder intentions, despite the seeming drawbacks?

Sources/Additional Readings:

Stealth Health for Kids – Newsweek

Lunch Line Redesign – The New York Times

New center, with $1 million grant, aims to make school lunchrooms smarter – ChronicleOnline, Cornell University

Daniel Kahneman: The Riddle of Experience vs. Memory – TED Talks

Dan Ariely: On Our Buggy Moral Code – TED Talks