FACULTY FEATURE: Jen-Wei Linn

April 26th, 2019 in Features 0 comments

The graininess of a film camera may seem old-fashioned in today’s world. With the digital 4k resolution cameras we have now, why would someone continue to use this much more outdated version? Wouldn’t they want to modernize and take much clearer photos? Dr. Jen-Wei — one of Boston University’s most innovative neurophysiologists — will turn down the digital cameras, as he prefers the originality and freedom of the film camera.

From Taiwan, Dr. Lin’s journey to BU is quite an amazing story. At National Taiwan University, Dr. Lin earned his Bachelor’s degree in Zoology in 1978. After this, Lin served in the Taiwan military service for three years. Following his service, he made the journey to SUNY – Buffalo, where he would complete his Ph.D. in physiology.

“At the time,” Lin said, “Neuroscience was mainly neurophysiology and neuroanatomy. When I began [my studies] in neurophysiology, I burned quite a few things,” Lin chuckles. This was fascinating for Lin as he describes the minute details of studying the traces of neurological processes and channels. Dr. Lin explains that neurophysiology allowed him to make the connections between these processes, which was much more interesting to him than other biological phenomena.

Dr. Lin first entered research in a lab studying a three synapse reflex in goldfish. Specifically, Lin focused on the synaptic transmissions among the multi-neurons along the spine.

“This was very interesting because this was one of the cells in the central nervous system that had multiple synapses,” Lin described. Very uniquely, Lin points out the inhibitory synapses that occur within these cells.

Dr. Lin then transitioned to New York University where he would complete his Ph.D. fellowship at the medical center. Here, Lin studied the giant synapse of both crabs and squids. Lin focused specifically on the depolarization of the neuron of the crab when its muscle would extend or contract for the majority of the year, but waited until summer when “squid season” would begin to work on his squid experiments.

It was after this when Dr. Lin then came to Boston University to begin as a professor. Currently, Dr. Lin teaches BI445: Cellular and Molecular Neurophysiology. This course focuses on the cellular and molecular basis of neural excitability and synaptic transmission. In the course, students work to extrapolate molecular understandings of ion channels to higher brain functions including learning, memory, and sleep. In the course, he incorporates these ideas into studying crayfish to understand the effects of pesticides and antiepileptic drugs.

For Dr. Lin, getting involved in research means being proactive.

“Talk to different professors and other students about what they’re doing. Figure out what you’re interested in, and ask yourself, ‘Is this really what I want to do?’” He advises. Lin says that having “thick skin” is advantageous, as it’s important to “not get lost in the little things you do.” However, Lin explains, that reaching out and making yourself accessible to others is the way to find what you’re passionate about. To put it in his own words, “listen by not being overwhelmed by noise.”

All of this is easy to do at Boston University. Lin calls Boston “a great city,” attracting a large herd of amazing people. Lin suggests taking full advantage of the city, integrating yourself within the communities of not only BU but also the other universities and institutions that surround the city. To become more acquainted with the city, you may follow Dr. Lin’s suggestion and go for runs throughout Boston and Cambridge. Exploring the city and becoming more familiar with what is around you opens you up to Boston’s full potential.

In my conversations with Dr. Lin, his appreciation for the vastness of life was incredibly evident. It was fascinating to hear from this man who works with the most innovative neurophysiology techniques and the most cutting-edge microscopes, but also prefers the use of a grainy film camera in capturing photos of his life. But why?

“Like an artist choosing color between oil or pastel in their paintings, the film camera produces this unique visual of grains,” Lin explains. Lin describes the use of a film camera as “a choice,” that — like neurophysiology — gives him the freedom to put things together himself.

This form of art, both in his photos and his research, possesses an individuality that can be only Dr. Lin’s: a truly fascinating man.

Writer: Trey Moore

Editor: Stephanie Gonzalez

Glutamate Excitotoxicity and Ischemic Stroke

April 16th, 2019 in Uncategorized 0 comments

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Glutamate is the major excitatory neurotransmitter utilized by the human nervous system and is involved in many important neurological functions. Best known for its role in memory formation and Long Term Potentiation (LTP), glutamate signaling is crucial for healthy brain activity. Despite glutamate’s importance in our everyday lives, too much glutamate can actually kill neurons, leading to stroke and death. This phenomenon is known as glutamate excitotoxicity.

In the synapse, a gap between two neurons, the presynaptic neuron releases neurotransmitters such as glutamate onto the receptors of the postsynaptic neuron. Glutamate will bind to two types of receptors on the postsynaptic neuron:  ionotropic glutamate receptors (iGluRs) and metabotropic glutamate receptors (mGluRs). iGluRs are the most well-known receptors through which glutamate exerts its effect. mGluRs can either upregulate or downregulate the effects of glutamate signaling based on their receptor type. The mGluRs deserve a separate blog post due to their complex mechanisms, and this post will focus exclusively on iGluRs in glutamate excitotoxicity.

Glutamate will activate two types of iGluRs: AMPA and NMDA receptors. In a healthy synapse, a regulated amount of glutamate is released from the presynaptic neuron with a concentration high enough to elicit a response in the postsynaptic neuron but low enough to not cause cytotoxicity. Activation of AMPA receptors allows sodium ions to flow into the postsynaptic neuron, depolarizing it. With enough depolarization, the intracellular positive charge forces a magnesium ion out of the pore of an activated NMDA receptor, allowing sodium ions and calcium ions to flow into the neuron. The calcium ion influx is involved in many signaling cascades including activating phosphorylating proteins, regulating gene transcription, recruiting more AMPA receptors to the postsynaptic density, and inducing dendritic spine growth. All of these changes strengthen the synaptic communication between the two neurons. This glutamate dependent mechanism is characteristic of a phenomenon known as long term potentiation (LTP) and is involved in the neurobiology of memory formation in the brain.

Glutamate excitotoxicity occurs when too much glutamate has been released into the synapse. A common mechanism through which this occurs is seen in ischemic stroke. In ischemic stroke, arteries supplying oxygen rich blood to the brain are blocked or narrowed, significantly reducing oxygen delivery. Without oxygen, ATP levels within neurons drop significantly. This is a crucial step in glutamate excitotoxicity due to ATP’s overall negative charge. With less ATP, the interior of the neuron becomes less negatively charged and more positively charged. This unwanted increase in positive charge forces open voltage gated calcium ion channels. An unnecessary influx of calcium ions into the presynaptic neuron causes the release of excess glutamate into the synapse. This excess glutamate overstimulates postsynaptic glutamate receptors, especially NMDA receptors. Abnormally high levels of calcium ions then flood the postsynaptic neuron, activating cytotoxic enzymes including proteases, nucleases, and caspases which proceed to destroy the neuron.

As if things could not get any worse, the damage does not stop with just one neuron. When the neuron dies it releases its own supplies of glutamate throughout the brain, in turn overstimulating and killing other neurons. Glutamate excitotoxicity has now extended its influence from a few neurons to many more neurons in the brain. This vicious cycle of excess glutamate release and neuronal death repeats itself over and over again in a matter of minutes, leading to the characteristic symptoms of stroke including facial drooping, distorted speech, and limb weakness. Without immediate medical intervention, the stroke patient will die within hours. Even with treatment the damage is already done; many stroke survivors are left permanently debilitated and can never return to a healthy, functioning life.

The intricate mechanism of ischemic stroke in all its lethal glory reverberates the old adage that too much of a good thing can be a bad thing. Understanding how glutamate excitotoxicity works is still under intense research, and many questions are still left unanswered. One thing is for sure: more knowledge about glutamate excitotoxicity has far reaching applications in medicine and neuroscience, with the potential to save countless lives.

Writer: Richard Kuang

Editor: Nathaniel Meshberg

Sources:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3985770/

https://www.rndsystems.com/resources/articles/neuronal-death-glutamate-excitotoxicity-protein-mediators-strategies-inhibition

http://www.ajnr.org/content/22/10/1813

https://www.ncbi.nlm.nih.gov/pubmed/14552898

https://www.ncbi.nlm.nih.gov/books/NBK6556/

https://www.mayoclinic.org/diseases-conditions/stroke/symptoms-causes/syc-20350113

 

 

FACULTY FEATURE: Robert Stern

April 12th, 2019 in Features 0 comments

While juggling the various responsibilities of college life, many undergraduates dream of a well-defined career path with straightforward steps to a successful life. However, life is always full of uncertainties, and that seemingly direct path may quickly reveal itself as a winding road. Dr. Stern is no stranger to this unexpected occurrence, but he prefers to embrace the serendipity of it:

“A winding path is a bit more of an adventure-- it’s also a little more fun.”

Dr. Stern’s own path has taken him through numerous academic institutions and places of employment up and down the East Coast. His journey has presently brought him back to Boston as a prominent professor and researcher at the Boston University School of Medicine (BUSM). Dr. Stern is one of the most influential research scientists in the field of Chronic Traumatic Encephalopathy (CTE), a neurodegenerative disease which plagues the brains of many NFL players today, as well as others with a history of repetitive blows to the head.

Growing up, Dr. Stern had wanted to be either a physician or a Broadway star. While applying to colleges, he searched for a school where he could potentially pursue both of his dreams. Ultimately, he decided on Wesleyan University. Though he settled for a major in biology and was determined to become a surgeon, a presentation by noted Harvard physician Dr. Herbert Benson – one of the pioneers of the Mind/Brain movement -- swayed Dr. Stern to the brain sciences.

After changing his major to Psychology and planning to conduct his senior thesis on loneliness and heart disease, he had to shift gears because his mentor suddenly left the school.  He then found another advisor, but changed the focus of his thesis to loneliness and its relationship to depression. During this time, he noticed a general lack of mental health support for the student population at Wesleyan. Inspired, he co-founded and directed a college peer counseling hotline he named ‘8-to-8’. The project was one of the first of its kind in the country (and is still in existence almost 40 years later), and played a role in Dr. Stern’s desire to work more closely with people.

While Dr. Stern helped others make the connections they needed, he himself ended up reconnecting with a former high school classmate, Ruthanne. Out of the blue, she contacted him seeking advice on her possible transfer to Wesleyan. Through a long phone call and a meeting over drinks, he convinced her to join him in Connecticut. Their discussions unknowingly signified the start of their romance as Ruthanne and Dr. Stern would eventually marry.

Following graduation from Wesleyan, Dr. Stern helped develop a similar peer counseling program at Andover High School for two years. And, during that time, he decided to dive into the emerging field of behavioral medicine. He was admitted to the Clinical Psychology doctoral program at the University of Rhode Island (URI) where he completed his master’s thesis in 1984 the progressive stages of cigarette smoking acquisition in adolescents. Unfortunately, it wasn’t the experience he had hoped for.

“I hated every second of it,” Dr. Stern laughs.

Feeling like he had gone down the wrong path, Dr. Stern decided to shift directions and join a practicum training program at a psychiatric hospital. The program was Dr. Stern’s first exposure to the field of neuropsychology. He enjoyed the experience so much that he decided to apply for a pre-doctoral internship at the Department of Veteran Affairs Medical Center in Boston. This highly competitive position was overseen by the late Dr. Edith Kaplan, a pioneer in clinical neuropsychology. Fortunately for Dr. Stern, he had connected with Dr. Kaplan previously while taking her classes at BUSM -- some of which he teaches today.

After securing the internship, Dr. Stern went on to grind out many 100-hour work weeks the following year. He then stayed on at the VA completing his dissertation research on depressive symptoms following stroke. The technology available at the time (CT scans were relatively new and MRI scans were not yet developed) restricted stroke localization to somewhat crude brain regions. But, even the ability to quantify moods like sadness in aphasic stroke patients lacking. In response, Dr. Stern developed the Visual Analog Mood Scale (VAMS).

“If it doesn’t exist, create it,” Dr. Stern said. “What started out as silly little drawings of a happy face and a sad face eventually turned into commercially published, standardized visual analog mood scales.”

As Dr. Stern was finishing his Ph.D., Ruthanne matched for her ophthalmology residency at Duke University. Dr. Stern managed to follow her southwards, moving to pursue a postdoctoral fellowship in neuropsychology and psychoneuroendocrinology from the University of North Carolina School of Medicine. Conveniently for them, the two universities sit only twenty minutes away (though during basketball season, the rivalry made the distance feel much further), and they eagerly took on their new positions. Dr. Stern was publishing and writing grants and getting grants and developing new areas of expertise. Chaos quickly overcame this eagerness when responsibilities piled on. Among the new responsibilities came parenthood, as Ruthanne gave birth to their two children -- a boy and a girl – one during residency and the other before fellowship training. Dr. Stern and Ruthanne moved closer to Boston when their youngest was one, and Dr. Stern found a new position at Brown Medical School.

A couple years after settling into their new home, Dr. Stern and his family were struck with somber news. Ruthanne had developed breast cancer. After a year of treatments, their lives returned to normal. Dr. Stern received several grants on topics ranging thyroid-brain relationships to HIV-associated brain disorders. He directed a memory clinic and a training program, and spent over 7 years developing a new, extensive neuropsychological test battery. However, after five years of health, Ruthanne had a recurrence of the cancer. A year and a half later, she passed away at the age of 43. Dr. Stern’s once-wonderful experience at Brown became dull in this troubling time. Funding was drying out, major collaborators were leaving or no longer available, and Dr. Stern was left a single parent with a long drive from Needham, a suburb of Boston, to Providence, Rhode Island. Yet while life was far from perfect, Dr. Stern’s children were healthy, happy, and wonderful and that was the most important thing.

Dr. Stern never believed he would encounter love again, but as his past shows, life constantly presented him with the unexpected. So it was without fanfare that a neighbor introduced him to a lovely woman named Susan. Although he had no intentions of pursuing her, their conversations revealed that they shared remarkably similar life experiences. Like Dr. Stern, Susan was a widow by cancer, and also the single parent of a boy and girl. Dr. Stern and Susan were able to develop a unique bond and mutual understanding of each other quickly fell in love. This beginning of a new chapter in Dr. Stern’s life allowed him to re-evaluate what brought him joy. Yet while Susan changed his life for the better, Dr. Stern’s disdain for his work in Rhode Island remained.

On a particularly bad day, Dr. Stern received a call from an old friend, Dr. Robert Green, asking if he would be interested in coming to work at Boston University School of Medicine. Dr. Stern jumped at the opportunity and was soon working with Dr. Green, running the Clinical Core of the NIH-funded BU’s Alzheimer’s Disease Center (BU ADC).

After giving a talk in Boston about Alzheimer’s disease one evening in 2007, Dr. Stern was introduced to former Harvard football player and WWE professional wrestler, Christopher Nowinski (now Dr. Nowinski), and jokingly explains that the two “kind of fell in love.”

At the time, although Dr. Stern had seen a couple of patients with dementia pugilistica (“punch-drunk” syndrome), he had not heard of the term CTE,. Dr. Nowinski had just formed the non-profit, Sports Legacy Institute (SLI, now Concussion Legacy Foundation) with world-renown concussion specialist and neurosurgeon, Dr. Robert Cantu. They were looking for a research institution to partner with and, as Dr. Stern was intrigued by what the study of CTE could do for advancing knowledge  about other neurodegenerative diseases and the potential impact on public health, they continued discussion about some form of affiliation. When Drs. Nowinski and Cantu asked if Dr. Stern knew of a neuropathologist who may be interested in studying the brains of deceased football players, Dr. Stern replied that he worked with a superb and highly respected neuropathologist at the BU ADC but he wasn’t sure if she would have that interest. Little did he know that, at the time, Dr. Ann McKee was a huge football fan and was also an expert in diseases involving tau protein, the same protein at the root of CTE. Dr. Stern called Dr. McKee and asked if she was interested. Dr. McKee was eager to join, and in the following months, Drs. Cantu, McKee, Nowinski, and Stern, with the support of Dean Karen Antman and others at the MED campus, founded the BU Center for the Study of Traumatic Encephalopathy, through a formal affiliation between SLI and BU.  As they say, the rest is history, with Drs. Stern and McKee becoming pioneers in the field of CTE research, increasing public awareness and forging major medical and scientific advances.

Dr. Stern is the lead principal investigator of a $16 million multi-center NIH grant (that was supposed to be funded originally by the NFL, but he doesn’t like to talk about that), has many other ongoing projects, is the director of clinical research for the BU ADC and BU CTE Center, has published hundreds articles, as well as two recent books . He particularly enjoys the dynamic nature of the Neurology Department at BUSM. Following his own advice, Dr. Stern has surrounded himself with nice people who make up his passionate, brilliant, and hard-working research team.

They are all “wicked smaht people,” Dr. Stern says jokingly in a fake Bostonian accent.

The approximately 15-member team works with Dr. Stern to conduct clinical research projects on AD and CTE within the department.

Although getting a grant funded or having a major paper accepted for publication is exciting, “if someone is really going to be a successful researcher, they have to enjoy the journey all along the way,” says Dr. Stern.

He explains that research is all about trying to answer a question -- and when the analysis comes back and supports the initial hypothesis, it is thrilling.

“When a paper gets published, even now, so many years into my career, I still get a little rush getting to see the paper with my name on it,” he adds.

Yet while he enjoys publishing his work, Dr. Stern does not forget to note the real drive behind his projects: “The most important part of it all are the people who I get to interact, the research participants, patients, and their loved ones. That also is what keeps me driving.”

Reflecting on his experiences, Dr. Stern urges current students to be open to new ideas and strive to create change in the world.

“If something is broken, fix it. And if there is a need for something and it doesn’t exist, make it,” said Dr. Stern. “Whenever I meet with anyone who has a can-do spirit, someone who says, ‘yeah, let’s do that,’ that is the most powerful type of person that I want to be around.”

For students pursuing research experience, Dr. Stern recommends reaching out to a lab and offering to help with anything.

“It really just starts with saying, ‘Hey, I’ll do anything,’ that’s really it,” he said. “If you can open the door by offering to do anything and then you prove yourself by being a nice person, a smart person, a hard-working person, then usually that turns into being able to move forward within a lab and to be offered more and more responsibilities,” said Dr. Stern.

Dr. Stern advises students to take time off after their undergraduate studies before applying to graduate or medical school.

“College is an amazing time and possibly not the time to make a final decision about what you want to do for the rest of your life,” said Dr. Stern.

He recommends spending at least two years in this capacity, permitting time to mature and gain valuable experience. He says it is really important to follow your gut and not feel stuck in one direction or another, while always doing something that excites you. His twists of fate enabled him to find his true passions and dedicate such a large part of his life to scientific innovation. Dr. Stern’s intricate career path exemplifies the advice he gives to current students:

“Realize that nothing is ever a finite decision.”

Despite his prominent role in academia, Dr. Stern puts in the effort to maintain a balance between his personal life and professional career.

“Make sure every day is filled with joy,” said Dr. Stern.

His own primary source of joy comes from spending time with his wife and four kids, along with their little cockapoo, Rosie. Boston also supplies Dr. Stern with positive energy: he relishes the diverse atmosphere, and as a self-proclaimed avid spinner, he cherishes the abundance of spin classes available. As for what the future holds, Dr. Stern looks forward to passing along his projects to his talented junior faculty and hopefully witnessing their developments lead to advances in neuroscience and to the benefit of public health.

Writers: Yoana Grigorova, Enzo Plaitano, Nicole Tacugue

Editors: Stephanie Gonzalez, Brian Privett

The role of physical exercise in preservation of the memory function.

March 30th, 2019 in Uncategorized 0 comments

Sports are increasingly widespread in modern-day American Academia. Perhaps, it is the plethora of research on healthy lifestyle, or the anticipation of the beach season, with sentiment ranging from apprehension to excitement to flatout morose ignorance, which we have to thank for this. Alternatively, it may be an amalgamation of those factors (and many others) that brought a drastic improvement of physical vitality as far as college students are concerned. In any case, there is more to it than good looks and capabilities to walk to the fifth floor of, for example, STH, rather than taking an elevator. Participating in some form of consistent physical exercise brings with it an improvement to the quality of memory later on in life, at least as far as men are concerned.

A study by an interdisciplinary group of scientists from Spain showed that long term exercise (35±15 years) promotes the preservation of memory function in middle-aged (47-67) men, specifically concerning the free immediate recall test and cued immediate recall test. The training (athlete) test-group showed a statistically significant increase in performance on both tests compared to the middle-aged sedentary group. Moreover, the number of weekly hours of exercise also showed a positive correlation with test performance. In short, continuous and consistent sports participation goes a long way when it comes to memory.

Having established the benefits for the middle-aged, it would have been nice if there was something in it for the young as well and there is! The very same study, also measuring common biological markers associated with memory impairment, such as plasma lipid peroxidation levels (MDA) and resting serum levels of BDNF, made a number of promising conclusions. For instance, both the middle-aged and young-aged (17-25) sedentary groups scored higher on the blood MDA levels (plasma malondialdehyde, a biomarker that correlates with oxidative damage) - which inversely affects memory. Moreover, a similar pattern (inverse correlation) is observed with BDNF (Brain-derived neurotrophic factor), except here the difference between the young sedentary and athlete groups is significantly higher. While BDNF is considered to promote neuronal growth, the researchers found no significant correlation between BDNF levels and memory test(s) performance but found a positive correlation between BDNF and MDA levels (which is bad). Thus, exercise does not only work for the middle-aged men but also the younger ones.

The most important part of this study is not, in all due technicalities, the uniqueness of its ideas, but rather its scope. Some studies have already shown the beneficial effect of exercise on people's memory, provided they are already suffering from certain conditions, such as Alzheimer's or mild cognitive impairment. Moreover, another set of studies explored the effect of short-term aerobic exercises, mostly targeting attention, decision-making and speed processing. Thus, this study is the first of its kind - exploring the connection between long-term exercise (not acute burst of activity) and memory in healthy men.

Finally, for the sake of objectiveness, limitations of the study should also be discussed. The most obvious drawback is the exclusion of women from the test groups, which subsequently makes this study only relevant for men (until proven otherwise). Moreover, the study itself is of a cross-sectional kind and hence is not impervious to various biases, such as cohort effects (in all due fairness, not many studies ever are).

So, guys, have you been hitting gym lately?

 

Writer: Ivan Kondratyev

Editor: Audrey Kim

Sources:

Baker, L. D., Frank, L. L., Foster-Schubert, K., Green, P. S., Wilkinson, C. W., Mctiernan, A., . . . Craft, S. (2010). Aerobic Exercise Improves Cognition for Older Adults with Glucose Intolerance, A Risk Factor for Alzheimer's Disease. Journal of Alzheimer's Disease, 22(2), 569-579. doi:10.3233/jad-2010-100768

Ferris, L. T., Williams, J. S., & Shen, C. (2007). The Effect of Acute Exercise on Serum Brain-Derived Neurotrophic Factor Levels and Cognitive Function. Medicine & Science in Sports & Exercise, 39(4), 728-734. doi:10.1249/mss.0b013e31802f04c7

Griffin, É W., Mullally, S., Foley, C., Warmington, S. A., O'mara, S. M., & Kelly, Á M. (2011). Aerobic exercise improves hippocampal function and increases BDNF in the serum of young adult males. Physiology & Behavior, 104(5), 934-941. doi:10.1016/j.physbeh.2011.06.005

Mueller-Steiner, S., Zhou, Y., Arai, H., Roberson, E. D., Sun, B., Chen, J., . . . Gan, L. (2006). Antiamyloidogenic and Neuroprotective Functions of Cathepsin B: Implications for Alzheimer's Disease. Neuron, 51(6), 703-714. doi:10.1016/j.neuron.2006.07.027

Rosa, A. D., Solana, E., Corpas, R., Bartrés-Faz, D., Pallàs, M., Vina, J., . . . Gomez-Cabrera, M. C. (2019). Long-term exercise training improves memory in middle-aged men and modulates peripheral levels of BDNF and Cathepsin B. Scientific Reports, 9(1). doi:10.1038/s41598-019-40040-8

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FACULTY FEATURE: David Somers

March 29th, 2019 in Features 0 comments

Dr. David Somers was in Kathmandu, Nepal, just about to head off for an expedition as part of his world travels, when he received an unanticipated phone call. Several professors had tracked him down in order recruit him to work on a project in the new Cognitive and Neural Systems Program at BU.

It’s no wonder that BU faculty went through the trouble to find Dr. Somers, as he can be best described as a modern Renaissance man. When he is not teaching Cognitive Psychology or conducting robust research, Dr. Somers enjoys travelling, craft beer, and ultimate frisbee. Although he has several seemingly distinct passions and hobbies, they somehow intersect and visibly manifest in his career.  

During his early educational endeavors, Somers states that there was no designated undergraduate path in neuroscience. Therefore, he pursued a degree as a math major and a psychology minor at Harvey Mudd College with the hopes of studying artificial intelligence in the future. Although Dr. Somers has an affinity for mathematics and computer science, he reoriented his focus towards neuroscience. “Physical sciences have become so hypothetical and estranged, but I was drawn to neuroscience because it is so important, huge, fascinating, and attainable,” he states. More specifically, Dr. Somers is particularly interested in how neuroscience is evolving with the rise of new technologies, and cites the importance of “learning the new methodologies and applying it to older philosophical questions regarding the mind.”

Following his undergraduate tenure, Dr. Somers moved on to a fellowship at MIT’s Department of Brain & Cognitive Sciences. There, he worked in a lab that specialized in rewiring neural circuitries in ferrets in order to restore sight. However, as a ethical vegetarian, he faced a moral quandary in utilizing animal models. He was then drawn to computational neuroscience to evade invasive animal work and transcend the limitations of animal models.

Around the same time, just one year before his doctoral dissertation, Dr. Somers witnessed the development of the fMRI machine and its nascent implementation in neuropsychological research. In alignment with his personal philosophy on keeping up with emerging technologies, Dr. Somers “went to grad school again to prepare, where [his] math background luckily transferred quite nicely.” When asked about the most surprising change he has observed in the field, Dr. Somers reflected upon the example of optogenetics, and likened its research atmosphere to that of the field upon the introduction of fMRI machines. He also reiterated the immense influence of technology on the constantly changing nature of neuroscience. “Keep learning new techniques--you may be doing your work in a field or methodology which doesn’t exist yet,” he states.

Currently, the excitement surrounding multimodal integration research inspires Dr. Somers, as hid lab specializes in investigating multisensory attention networks and visual science. He is interested in a multimodal approach in his laboratory, and seeks to explore how integration varies according to different types of stimuli. In his lab, he uses fMRI techniques to study the relationship between vision and attention, perception, and working memory. Dr. Somers also developed a five-finger glove for delivering tactile stimuli to further study sensory modalities.

As he reflects his exciting life as a BU faculty member, Dr. Somers is glad he received that coincidental phone call in Nepal. Even though he spends a lot of time shoveling snow, he still emphasizes his admiration for Boston. “My colleagues are hardworking and interesting people, and I enjoy my interactions with the students. They seem to be getting smarter and smarter, and increasingly passionate, which makes teaching here so fulfilling.”  For students interested in pursuing research, Dr. Somers offers two pieces of advice: “Find a question which you really love and care deeply about. Then learn the new methods and get after it.”

Writer: Safia Mirza

Editor: Brian Privett

It’s All in Your Gut

March 18th, 2019 in Uncategorized 0 comments

People have not placed enough importance on the functions of our microbiome and its effects on our personal health, since it is early in research and not well understood yet. The microbiome is the collection of microorganisms, including bacteria, fungi, and viruses, in our human body. Microbiome means all the genomes of microbes in an environment, while microbiota is supposed to mean the actual organism. Today many are using the term microbiome to mean multiple things, the microbiome, microbiota, and the activities of the microbiome in animals and humans. Microbiome having a broader definition, though not the correct usage of the word. The microbiome in the human gut has shown to have effects on the immune system, overall health, and metabolism in animals and humans. Celiac disease, obesity, type 1 diabetes, and many more diseases are observed in humans with a low diversity microbiome. One observation that is surprising is the effects of different types of gut bacteria on neurobehavior, specifically related to depression, anxiety, and a lower quality of life.

An experiment led by Professor Premysl Bercik with three groups of mice at McMaster University was able to correlate certain gut bacteria with symptoms of depression and anxiety. Two groups of mice, one with no bacteria in their gut in a sterile environment and one with a range of bacteria, were put under stress for 3-21 days. The control group had no bacteria and had not been put under stress. Both groups of no bacteria had no symptoms of depression, while the mice with the normal gut microbiomes showed symptoms of depression and anxiety. Both groups that were under stress had increased levels of corticosterone, a stress hormone, but only the group of mice with normal gut microbiomes showed symptoms. Proving the effects of microbes on neural behavior. Multiple cases have proven microbes affecting mental health in animal models, though little research has been done on humans. Professor Jeroen Raes, professor Sara Vieira-Silva, and their team compared the gut microbiome of 1,054 individuals diagnosed with depression in the Flemish Gut Flora Project at the University of Leuven in Belgium. They found certain bacterial genera depleted or abundant in these individuals. Two that stood out to be the most commonly depleted in these individuals were Coprococcus and Dialister. Raes and his team studied the genomes of bacteria from the human gastrointestinal tract and found that some had the ability to produce neuroactive compounds. They are currently creating a toolbox with computational techniques of what bacteria in the gut can affect neuroactive compounds and the mechanism behind it. An interesting one they found is the ability of the microbiome to produce DOPAC led to better mental health as its function is growing the neurotransmitter dopamine.

Scientists are studying the effects of the environment, food, processed foods, and medications on our microbiome and how the microbiome affects our health. Research of the effects of mental health in human models has now launched. This creates the possibility of treating depression and anxiety by changing people's microbiome in the future. Further research needs to be done in order to understand the mechanisms of how our microbiome affects our health and studying the microbiome of healthy populations too. For now, eat your probiotics and stay away from sugar and processed foods to diversify your microbiome for better mental health.

Writer: Lauren Renehan

Editor: Nathaniel Meshberg

Sources:

https://www.genengnews.com/news/depression-and-gut-bacteria-link-strengthened/ https://neurosciencenews.com/depression-gut-bacteria-10685/ https://www.iflscience.com/plants-and-animals/link- found-between-gut-bacteria-and-depression/ https://www.bmj.com/content/361/bmj.k2179

Image source

FACULTY FEATURE: Steve Ramirez

March 8th, 2019 in Features 0 comments

Any view from one of the offices near the top of the Kilachand Center for Life Sciences and Engineering building will leave you speechless. One particular office, with a baseball nestled amidst countless awards scattered about the desk, a bottle of celebratory champagne waiting to be popped open, and a giant inflated T-rex standing beside a whiteboard scribbled with complex calculations, tends to stand out from the crowd. This is the office of Dr. Steve Ramirez.

Dr. Ramirez is what you would call a “true Bostonian.” Growing up in Everett, MA, Ramirez decided to stay around the area by attending Boston University for his undergraduate career. However, he found a lot of trouble in deciding what he wanted to major in.

“I enjoyed everything,” Ramirez explained, “From physics to biochemistry to literature.” It wasn’t until he had a conversation with a familiar face of the BU community when he decided neuroscience was his fit. A conversation with Paul Lipton,  BU’s current undergraduate neuroscience director, eventually persuaded Ramirez to study the organ that had created everything he had a passion for, joining BU’s first graduating class of neuroscience majors.

After BU, Ramirez made the long journey across the Charles River to pursue his PhD at MIT. Here, Ramirez describes as “the best five years of my life.” Along with playing Mario Kart with his roommates whom he refers to his closest friends, Ramirez credits MIT with where he first got the inspiration in researching the interactions with memories.

Ramirez continues this research with his next long venture to Harvard University, where he completed his fellowship, serving as the “launchpad” of his own lab. Ramirez’s current research focuses on depression, anxiety, and PTSD, in which he is questioning whether it is possible to turn on positive memories - or turn off negative memories - to curing these diseases. This is done by tracking brain cells that respond to certain signals of light and then reactivating the cells to reproduce (or halt) the previous emotion, otherwise known as optogenetics.

At BU, Ramirez is the instructor for NE 337, Memory Systems of the Brain. This course works to study to neurobiological mechanisms of memory. By studying amnesia in humans and experimental models of amnesia in animals, the course is engineered to focus on evidence for multiple forms of memory and the distinct brain systems that mediate them.

The classes taught by Dr. Ramirez aren’t like your typical STEM courses. Ramirez makes it a priority to relate neuroscience to modern types of multimedia, basing his teaching methods off of a course he taught at Tufts called Neuroscience and Hollywood. It’s not uncommon for a homework assignment from Ramirez is to watch the Bourne Trilogy or Inside Out.

“A lot of stuff is wrong, but there are certain concepts they actually get right,” Ramirez explains. “The material has to be grounded in ‘why do I care?’” Ramirez answers as to why he assigns these films. “Of course there are also TED Talks and research articles, but I include these movies because they’re what I like to watch for fun.”

When asked how Ramirez likes working at BU, it was very evident the impact the community makes on him.

“At BU, the learning and memory community really are here to help in any way possible,” he begins, “Unlike other universities, research teams are not their own separate islands here.” Another important aspect Ramirez highlights is that “everybody actually has a real life and can enjoy life outside of the lab,” demonstrated through the Macaroni Mondays and Taco Tuesdays he partakes in with his peers.

For an undergraduate interested in getting involved in research, Ramirez suggests to reach out to professors and see if they could entertain having you in their lab.

“Not all research is going to interest you, but getting involved will help to determine what you are interested in.” Ramirez assures that it’s okay to not know exactly what you want to do with your neuroscience degree after BU. “Neuroscience is constantly changing, and with that, so are the opportunities. So the job you might have 10 years from now might not even exist today.”

This type of encouragement stems from the overwhelming adoration Dr. Ramirez feels for his parents, whom he continues to call twice everyday. “I owe them my life,” he explains, “Coming into the country illegally to give me a fighting chance at an education.” This sense of altruism is conveyed through his interactions with his students. “I want to see them fight through the tough questions science has to offer and succeed, and I genuinely think they will.” Ramirez credits his father with his sense of continued optimism.

“There’s a million different reasons to be angry in 2019, but there’s a couple worth celebrating,” Ramirez explains.

You are one of the few, Dr. Ramirez. Thank you.

Writer: Trey Moore

Editor: Emme Enojado

FACULTY FEATURE: Kathleen Kantak

January 25th, 2019 in Features 0 comments

While walking through the Laboratory of Behavioral Neuroscience, one cannot help but stare at the equipment and visualize the many restless nights dedicated to countless experiments. Maybe it’s the abundance of hanging lab coats or the many apparatuses waiting to be used, but the lab brims with an addictive dose of excitement and ambition. This energy sources from the persistent and determined Dr. Kathleen Kantak, the fearless leader of this captivating space.

Dr. Kantak’s countless publications and long line of accolades provokes intimidation. However, the hesitation to make her acquaintance dissipates as her whimsical personality surfaces. Her office -- a small space reminiscent of a snug personal library -- is thought provoking and engaging. She unveils her story naturally, and the space seems warmer.

For Dr. Kantak, it started with a cranial fish dissection during her freshman year of high school.

“I was so enthralled by what I was seeing that I didn’t even notice I had also cut myself,” she said.

The experience of seeing a brain for the first time inspired her to pursue neural studies, and though she never imagined going into medicine or conducting clinical trials, she wanted to make a worthy contribution to society. Thus, after earning a degree from Potsdam State University, Dr. Kantak completed a Ph.D. in Biopsychology at Syracuse University, where she focused on neural control in consummatory behavior through animal models. Her post-doctoral studies -- at The University of Wisconsin (Madison) and Tufts University, respectively -- focused on studying aggression from the behavioral physiologist and pharmacological perspectives.

Dr. Kantak began working as an Assistant Professor at Boston University in 1982, the same year that she founded the Laboratory for Behavioral Neuroscience. Building a lab from scratch was no easy feat: grants were limited to very few researchers and the Neuroscience program was yet to be created.

“There was no neuroscience when I started… the entire department has grown tremendously over time, it has been fascinating to watch” she said.

Her work, however, proved relevant to the times. During the late 1980s, cocaine abuse emerged as a serious concern to the medical and public health worlds. This inspired Dr. Kantak to investigate the various aspects of this particular drug addiction.

Since there is no substantial treatment or FDA approved drug for cocaine dependence, Dr. Kantak’s efforts have been relentless. She has investigated both the pharmacokinetic and pharmacodynamic ways that cocaine works in the body, as well as potential drugs for therapeutic use of addiction.

Although the majority of the research she has conducted involves cocaine, Dr. Kantak has also pursued studies on animal models of ADHD. Unsurprisingly, she ended up connecting the ADHD research to cocaine as a way to study comorbidity.

“I guess I just have a high affinity for cocaine research,” she said with a smile and a laugh.

Additionally, Dr. Kantak investigates polysubstance abuse, analyzing the relationship between heroin and cocaine addictions. In her lab, she has enlisted the help of other renowned researchers originating from an array of specialties such as molecular biology, neurochemistry, and clinical research. Although her work is based on animal models of addiction, she works closely with clinical researchers and physicians to move her work one step closer to human subjects.

Today, the tenured Dr. Kantak is not only the director of the Laboratory for Behavioral Neuroscience, but she also holds an appointment as a Lecturer at Harvard Medical School in the Department of Psychiatry (Psychobiology) as well as at the Division of Behavioral Biology at the New England Primate Research Center.

At BU, Dr. Kantak currently teaches NE/PS333: Drugs and Behavior, one of the elective courses for undergraduate neuroscience majors. Her course focuses on understanding the action of drugs on the brain in order to understand how these drugs influence behavior.

Writer: Heidi Santa Cruz 

Editor: Emme Enojado and Stephanie Gonzalez 

Less Sleep, Less Friends

December 11th, 2018 in Uncategorized 0 comments

Interestingly enough, in today’s society, it seems like depriving oneself of sleep is almost like a trophy to jokingly brag as people attempt to see who slept the least number of hours yesterday or who pulled the most number of all-nighters last week. In addition, with finals season approaching, it becomes tempting for most students to sacrifice their sleep to score a few more points on the exam, although one can’t help but to ask if it was really worth it. Sleep deprivation seems like a necessary part of life that many college students must go through to succeed academically. There is even a joke that college students can only choose two of the following: good grades, social life and enough sleep. However, one of the choices, social life, seems unlikely as a sustained pattern of sleep deprivation can have an impact on the social aspect of our lives.

A study conducted in UC Berkley showed that people who suffer from sleep deprivation tend to become recluse; instead of seeking protection from society, sleep deprived individuals withdraw from social situation in the hopes of obtaining rest. In this experiment, they showed participants a stranger with a neutral facial expression walking towards them, and they asked them to hit the panic button when they felt that the stranger was getting too close. They found that sleep deprived participants hit the button significantly earlier than those who did get sleep. Through fMRI scans, they tried to see what regions of the brain were responsible for this behavior. One region, called the near space network, was very active compared to the control group. This region allows one to orient oneself in space and get out of threatening situations that involve spatial elements. In addition, the theory of mind network, which allows people to interpret others’ intention, was less active in sleep deprived participants than the control group. Thus, sleep deprivation may lead to a more antisocial attitude and an inability to fully detect social cues.

Yet another study also shows increased anxiety and fear levels in people who suffer from sleep deprivation. Sleep deprivation can increase sensitivity in the amygdala, leading to stronger fear responses to a stimulus. As a result of the activation of the amygdala, the ventromedial prefrontal cortex (vmPFC) begins to regulate emotion and inhibit activity in the amygdala. Another area of the brain, the insula, does the opposite of vmPFC and increases the activity in amygdala which then leads to fear acquisition. In a study by Feng et al. (2017), participants’ brains were tracked with an fMRI while they were shown series of different shapes in which a certain consecutive pattern of shapes would indicate an electric shock. In sleep deprived participants, higher activity was seen in the connections between the amygdala and the insula, while for the control group a higher activity was seen between amygdala and vmPFC.

When comparing the results of the two studies, both makes sense; sleep deprived individuals have increased levels of anxiety and fear which could have led to earlier responses in pushing the panic button. Both studies also demonstrate that the lack of sleep can affect one’s mood and thus their ability to socially interact with others. Although it is difficult for college students to find time to get quality sleep, getting sleep can possibly improve the social aspects of one’s life.

Writer: Audrey Kim

Editor: Lauren Renehan

Sources:

https://www.inverse.com/article/48046-sleep-deprivation-leads-to-social-isolation-in-new-study https://psychcentral.com/blog/how-being-sleep-deprived-alters-a-brain-connection-that-causesfear-and-anxiety/

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Deep Brain Stimulation

November 27th, 2018 in Uncategorized 0 comments

Over the past two decades, a neurosurgical technique known as Deep Brain Stimulation (DBS) has revolutionized the fields of both medicine and neuroscience. DBS has been able to accomplish incredible feats once deemed impossible, one of these being the extremely effective treatment of Parkinson’s Disease symptoms. DBS has also opened many doors to a bright future where debilitating neurological disorders and diseases may be eradicated.

So what exactly is Deep Brain Stimulation? Deep Brain Stimulation essentially consists of sending electrical impulses to certain brain areas via surgically implanted electrodes, resulting in the removal of adverse neurological symptoms. The exact mechanism by which DBS exerts its effect on neurons is still not fully understood, although many theories have been presented. One popular explanation for the mechanism behind DBS is that electrode stimulation of certain brain areas induces changes in neuronal activity in the respective neural circuits that would ultimately change physiological and cognitive behavior.

An example of DBS in action can be seen through one of its most common applications, Parkinson’s Disease treatment. Parkinson’s Disease is characterized by voluntary motor deficits and symptoms including resting tremor, bradykinesia, postural instability, extreme difficulty initiating voluntary movement, and more. These symptoms are caused by the loss of dopamine producing neurons in an area called the substantia nigra, which is a constituent of a much more complex brain circuit within the basal ganglia that controls the initiation of voluntary movement. Needless to say, this neurodegenerative disease is very debilitating for the patient. When medications such as L-DOPA fail to alleviate Parkinson’s Disease symptoms, DBS steps in to save the day. Electrodes are surgically inserted into brain areas such as the internal Globus Pallidus or the Subthalamic Nucleus and are connected to an internal pulse generator (IPG) located in the patient’s chest or abdominal cavity. Upon the initiation of electrical impulses to those certain brain areas via the implanted electrodes, the patient’s symptoms disappear immediately and the patient is able to execute normal voluntary motor function without difficulty.

DBS holds vast potential and unending applications in the fields of medicine and neuroscience. DBS research is currently being done to investigate its effect in treating a plethora of neurological disorders including major depressive disorder, OCD, PTSD, addictions, Alzheimer’s Disease dementia, chronic pain, schizophrenia, eating disorders, and more. As mentioned, DBS has opened the doors to a new and hopeful future in which neuroscience research and medicine can eradicate the most debilitating of neurological disorders. Ironically, although DBS was created to provide an answer to the many questions plaguing neuroscientists and doctors today, it has instead prompted us to ask infinitely more questions and has further shown how little we know about our own brains. I will end our short discussion of Deep Brain Stimulation with a quote by Santiago Ramon y Cajal, the father of modern neuroscience himself, which sums up what DBS, and neuroscience itself, is all about: “To know the brain...is equivalent to ascertaining the material course of thought and will, to discovering the intimate history of life in its perpetual duel with external forces.”

Writer: Richard Kuang

Editor: Audrey Kim

Sources:

https://www.sciencedaily.com/terms/deep_brain_stimulation.htm

https://www.ncbi.nlm.nih.gov/pubmed/18540149

https://www.ncbi.nlm.nih.gov/pubmed/26788743

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