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Videos from our fall events are now online, in case you missed them or want to revisit the events. Videos are embedded below (when possible) and all are permanently archived in our media library.

 

2015 Iscol Lecture:
Workforce of the Future

October 7, 2015
Reshma Saujani, Founder and CEO, Girls Who Code

 

 

2015 Bronfenbrenner Lecture:
The Obama Evidence-Based Revolution: Will It Last?

September 16, 2015
Ron Haskins, Center on Children and Families; Budgeting for National Priorities; Economic Studies, Brookings Institution

 

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Talks at Twelve: Barbara Ganzel, Thursday, September 10, 2015

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Trauma-informed Hospice and Palliative Care: Unique Vulnerabilities Call for Unique Strategies
Barbara Ganzel, Visiting Fellow, BCTR

Thursday, September 10, 2015
12:00-1:00PM
Beebe Hall, 2nd floor conference room

Hospice and palliative care populations may be uniquely vulnerable to trauma and stress-related disorders. Trauma reactivation due to normal aging may combine synergistically with medical trauma at the end of life, particularly in the presence of chronic pain, anxiety, delirium, or dementia. This in turn will negatively impact patient mental health, well-being, and reported pain, with important consequences for patient care. Assessment of prior trauma is recommended in hospice and palliative care, along with the development of trauma treatment strategies appropriate to these populations.

In her talk Dr. Ganzel will share some of her findings and observations learned from her work at Hospicare of Ithaca.

 

After receiving her Ph.D. in Human Development at Cornell, Barbara Ganzel did postdoctoral work in integrative neuroscience at the Sackler Institute at Weill Cornell Medical College in NYC. Her pre- and post-doctoral research was supported by National Research Service Awards from NIMH to study trauma-related sensitization of the stress response in nonclinical populations. She continued this work as director of the Lifespan Affective Neuroscience lab at Cornell. In 2013, she entered a clinical respecialization program to focus on stress/trauma at end-of-life. Dr. Ganzel currently works with a national collaboration of clinicians to develop palliative treatments for trauma, anxiety, and pain in hospice patients.

 

This talk is open to all. Lunch will be served. Metered parking is available in the Plantations lot across the road from Beebe Hall. No registration or RSVP required except fo groups of 5 or more. We ask that larger groups email Patty at pmt6@cornell.edu letting us know of your plans to attend so that we can order enough lunch.

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Life and the Adolescent Brain

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Reflection on our own adolescent years may include memories of excitingly risky activities or profound emotional vulnerability, or both. Risk and vulnerability are at the heart of two critical themes in research on adolescence. Adolescence is a period of heightened risk-taking behavior (Steinberg, 2008) and it is also the peak developmental period for the onset of psychological disturbance (Paus, Keshavan, & Giedd, 2008). However, a third theme in research on adolescence is at odds with these stereotypes of teenage emotional chaos and out-of-control behavior. This third theme highlights youth resilience and the ability to adapt and thrive in the expanding social world of the teenager (Crone & Dahl, 2012). Neuroscience unites these three themes by shedding light on the peculiarities of the adolescent brain and their impact on behavior. To understand adolescent behavior, it is helpful to look at what is happening in the adolescent brain – and this is a story that begins much earlier in life.

In the developing human brain, there is a massive early overgrowth in the number of connections or synapses between neurons (thus allowing a high degree of malleability in the brains of the very young). This early overabundance of synapses is countered by two major bouts of synaptic pruning, the first of which occurs in early childhood (around age three) and the second of which occurs during adolescence. Pruning drives a 50 to 55% decrease in the number of synapses across the entire cortex between late childhood and early adulthood. This cortical thinning is a marker of brain maturation and is associated with more adult-like cognitive abilities.

During pruning, any neural connections that have not been consistently used are eliminated. Thus, when we were adolescents, pruning served to streamline the efficiency of networks of neurons that we used most often. Our brains were sculpted to fit our own particular environment (a real life example of “you are what you do”). At the same time, increasing thickness and density of fatty white matter (myelin) served to insulate the “wiring” between neurons. This effectively boosted transmission power across the long connections in the brain that underlie the extended neural networks responsible for complex thought and behavior. Thus, during adolescence and young adulthood, pruning and myelination worked together to establish and strengthen the higher-order neural networks that we use for planning and regulating what we do.

Different brain areas develop at different rates and the prefrontal cortex (PFC) is among the last brain regions to mature. This is not surprising, since it is the most interconnected area of the brain. The PFC is referred to as the ‘C.E.O’ of the brain since it is involved in executive functioning. These executive functions include planning, decision making, and direction of working memory, i.e., the ongoing thought processes that allow us to complete tasks and plan for the future. The PFC is capable of promoting such complex human thought because of its connections with other members of the brain community. Within the adolescent PFC, pruning and myelination are creating big improvements in the fine-tuning of local connections, as well as profoundly strengthening its long-distance communications with the rest of the brain. These long-distance connections form the integrative neural networks responsible for higher level processing such as self-perception and goal-directed behavior, and so they are crucial to making rational decisions and regulating emotional drives. These “smart circuits” finish their development last because they are continuously refined and polished across adolescence and young adulthood. This is a big factor in the unique way that adolescents process their experiences and navigate their environment.

First, there may be a lag in the connections between the PFC and those regions of the brain devoted to motivated, reward-seeking behavior. A substance in the brain called dopamine is the primary chemical signaler in this network. During adolescence, there are excessive levels of dopamine in these regions, leading to increased activation of these reward systems. In turn, adolescents demonstrate elevated exploration and reward-seeking behavior. There is neuroimaging evidence that the adolescent PFC is not yet able to effectively inhibit this increased reward-seeking. These ‘rewards’ that an adolescent is after could be anything from drugs and alcohol to social acceptance. In the pursuit of the positive feelings driven by this circuitry, teens may drink, do drugs, or have unprotected sex.

The PFC has strong connections to brain regions that underlie emotion processing. These are areas of the brain that direct our survival-related behaviors (sometimes called “the four F’s” – feeding, fight, flight, and sex). These circuits also underlie the formation of social bonds, which have been key in our evolutionary history of overcoming hardships through group cooperation. These brain regions initiate pleasant emotional states of desire, as well as negative feelings when we feel fearful, ashamed, or rejected. When these ‘higher order’ social networks include a mature PFC, they allow us to behave effectively in social situations. The PFC guides our attempts to impress and comfort others, to empathize, and to having deeply meaningful exchanges with our fellow man about what we experience.

Neuroimaging technology allows scientists to measure activity within the neural circuits that underlie these behaviors. In one study, adolescents saw pictures of emotional images, such as the disapproving or angry face of a peer, while their brains were being imaged in a magnetic resonance imaging (MRI) scanner. Those adolescents who were less resistant to peer pressure showed evidence of weak connections between their prefrontal cortex and their reward areas, and those who were more socially resistant showed stronger, more mature connections between these areas. The authors of the study concluded that socially resistant adolescents were better able to recruit their PFC to help them regulate their emotions when faced with negative social information. It was suggested that this, in turn, may allow these young people to resist social pressure to engage in risky behavior (Grosbras et al., 2007).

Adolescents are more attuned to how others respond to them, picking up on subtleties of social exchanges and attributing meaning to them. They tend to be highly sociable and sensitive to acceptance and rejection from peers -- more so than children or adults. This social intensity may be due, in part, to higher adolescent levels of another chemical signaler, oxytocin, a hormone that enhances social emotions in mammals. A mature PFC is more able to modulate social highs and lows associated with social acceptance and social rejection. The still-developing adolescent PFC is less able to do so, so that a social threat is more likely to initiate the neural and hormonal cascades and negative feelings that we experience as stress. For example, an adolescent girl may angst over the details of exchanges with boys. Another teen’s self-esteem may be decimated by being picked last in gym class. Happily, this increased sensitivity to the social world may also allow social support to have an elevated beneficial effect for teens experiencing stress. For example, research on social buffering investigates how the presence of supporting and comforting others can help to decrease the intensity of the stress response and its associated negative feelings. These studies find that social buffering effects are amplified during adolescence, so that teens more readily absorb the positive effects of social support in the face of stress (Buwalda, Geerdink, Vidal, & Koolhaas, 2011). This finding suggests that interventions that enhance healthy social buffering may be particularly helpful for our stressed teens.

Adolescent brain development provides some insight into why adolescents take more risks, have increased odds of experiencing psychological distress, and rely heavily on peer approval. It has been argued, though, that study of the adolescent brain has done more to reveal that this developmental period is ripe with opportunity. Although the adolescent PFC is less efficient in inhibiting emotionally-driven impulses, a new line of research suggests that this very lack of maturity allows greater cognitive and social flexibility (Crone & Dahl, 2012). Not only is the adolescent brain is still changing and adapting to environments, it is able to more quickly switch attention to novel social features of the environment. This gives adolescents an advantage in navigating their complex social worlds, and in creatively pursuing new friendships and connections. Thus, neuroscience tells us that the adolescent brain is not merely immature, but rather it is perfectly suited to foster exploration of new environments, soak up the benefits of social closeness, and mold future adult capabilities.

 

Dr. Barbara Ganzel, Director, Laboratory for Lifespan Affective Neuroscience
blg4@cornell.edu

 

 

Sarah Moore, graduate student, Human Development

 

 

 

 

References

Buwalda, B., Geerdink, M., Vidal, J., & Koolhaas, J.M. (2011). Social behavior and social stress in adolescence. Neuroscience & Biobehavioral Reviews, 35(8), 1713-1721.

Crone, E. A., & Dahl, R. E. (2012) Understanding adolescence as a period of social-affective engagement and goal flexibility. Nature Reviews Neuroscience, 13(9), 636-650.

Grosbras, M., Jansen, M., Leonard, G., McIntosh, A., Osswald, K., Poulsen, C., & Paus, T. (2007). Neural mechanisms of resistance to peer influence in early adolescence. The Journal of Neuroscience, 27(30), 8040-8045.

Paus, T., Keshavan, M., & Giedd, J. N. (2008). Why do many psychiatric disorders emerge during adolescence? Nature Reviews Neuroscience, 9(12), 947-957.

Steinberg, L. (2008). A social neuroscience perspective on adolescent risk-taking. Developmental Review, 28(1), 78-106.

BCTR Resources on adolescent neurology

Video of talks on the adolescent brain from the 2011 Bronfenbrenner Conference, The Neuroscience of Risky Decision Making, are available here. They include:

• Eveline Crone, Adolescent Brain Development: A Window of Opportunity for Learning and Social Cognition
• Jay Giedd, The Adolescent Brain: New Views from Neuroimaging
• Beatriz Luna, Adolescent Risk Taking: Immaturities in Cognitive Control and Reward Processing

Also see the recent book The Adolescent Brain co-edited by BCTR faculty affiliate Valerie Reyna and published by the American Psychological Association.

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BCTR welcomes visiting fellow Dr. Chiyoko Kobayashi Frank

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The Bronfenbrenner Center for Translational Research is hosting Chiyoko Kobayashi Frank, Ph.D. as a Visiting Fellow (October 1, 2012 – September 30, 2013). Dr. Frank will collaborate with Dr. Barbara Ganzel, a faculty affiliate of the Bronfenbrenner Center, and be housed in Dr. Ganzel’s Lifespan Affective Neuroscience Lab - which is presently in G88 Martha Van Rensselaer Hall. Dr. Frank received her Ph.D. from the Department of Psychology at Cornell University in 2007 and she is currently an adjunct member of the clinical psychology faculty at Fielding Graduate University, Santa Barbara, CA. Dr. Frank is collaborating with researchers affiliated with the BCTR on a project in the area of translational human neuroscience. They will submit the results of this project for publication, with the hope of contributing to the advancement of scientific understanding of sources of social risk and maladaptation in children and adults.

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What’s the brain got to do with it?

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What is translational neuroscience? The new field of translational neuroscience uses brain science to inform applications that improve health and well-being. This means using (or improving) our understanding of the brain in order to develop new strategies for intervention. Until recently, translational neuroscience has supported medical interventions that are clinic-based, as in pharmacological, surgical, or behavioral treatments for neural and neuropsychiatric disorders. New on the horizon, however, is the use of neuroscience perspectives to inform social and behavioral interventions that are ecologically-based and can be delivered in the home or school setting. The target of these interventions has expanded to include developmental health outcomes, school readiness, and health promotion, in addition to brain-based disorders. This new approach takes translational neuroscience out of the clinic and puts it to work in our communities.

This series of short articles will present some of the possibilities inherent in this new perspective on translational neuroscience. We invite you to join us in exploring the promise of this approach.

What’s the brain got to do with it? Everything. This is because the brain is the critical mechanism linking the presentation of a stimulus and production of a complex behavioral response. Let’s say that you suddenly see a tiger bounding down the sidewalk in your direction. Your brain processes the sensory information: the stripes, the snarl, the catness, and the size of the approaching animal. Your brain interprets this information as danger and produces a survival response – your heart races, your blood pressure spikes, and you dive into the nearest open doorway. Without the neural processing of sensory input, you cannot be aware of your danger (the sight and sound of the oncoming tiger) or the possibility of escape (the open doorway). Without the brain’s emotional and cognitive processing of this sensory information, you cannot mobilize your body’s emergency energy resources or plan your own rescue. Without connections between your brain’s motor processing systems and your muscles, you cannot produce life-saving behavior. Without a brain, you are tiger food.

Not only is your behavior affected by your encounter with the tiger, so is your brain and the rest of your body. In large and small ways, your brain is impacted by life events and by your environment, and this, in turn, affects what you do and how your body works. Research has demonstrated that major, potentially traumatic stressors (such as tiger attacks) may have long-term effects on brain structure, brain and body function, and behavior -- even after just one event (Ganzel et al., 2008). Other work has demonstrated that more subtle, pervasive, and/or chronic stressors (such as poverty or growing up in a chaotic household) can also impact your brain and body - including decreasing your immune response (Gianaros et al., 2007; Taylor et al., 2006).

The brain, stress, and health. Whether stress comes in a single awful episode or a chronic grind, research has demonstrated that there is a strong link between stress and poor health. Recent thinking identifies the brain as a big part of that link (Ganzel et al., 2010; McEwen, 2007). Research suggests that stress can cause “wear and tear” in the brain areas most responsive to stressors; these are the brain areas that are on the front lines of saving your life from the tiger or keeping you going during the long illness of a loved one. Over time, the “wear and tear” in these regions can reshape your brain. In doing so, it is reshaping your body’s response to the next stressor.

For example, there is expanding evidence that accumulated stress decreases the size of the human prefrontal cortex in areas that underlie executive function, even in people who do not have a mental disorder (Ansell et al., 2012; Ganzel et al., 2008). These particular brain areas serve as the “air-traffic control” for emotion, cognition, and behavior, so that emotion regulation, cognitive control, and behavioral inhibition are likely to be affected. These brain areas also regulate physiological stress responses in the periphery of the body, including stress-related changes in heart rate, blood pressure, and immune function (Lane & Wager, 2009).

We are only beginning to learn what happens when stress remodels these brain areas. However, this work is likely to shed light on the mechanisms that link cumulative risk and cognitive impairment, neighborhood violence and child social-emotional adaptation, poverty and ill health, among very many important questions. An understanding of the impact of environmental risk on the brain may be a critical step towards improving and assessing existing therapeutic interventions, and developing new, better-targeted ones. This is important new ground for translational neuroscience.

Vulnerability and opportunity in the developing brain. We are learning more every day about how the brain works, how it develops, and how its development affects how it works.

In humans, the central nervous system begins to form during the first few months of fetal development. At birth, the human brain has approximately 100 billion neurons (about as many neurons as there are stars in our galaxy). Although all neurons develop through the same stages, different brain regions develop according to different timetables. For example, maturation in the frontal cortex starts in the motor area (involved in the execution of bodily movement) and ends with maturation of the dorsolateral prefrontal cortex (DLPFC) in early adulthood (Giedd et al., 1996). The DLPFC is a high-level association area and is one of those brain regions that play a critical role in planning, executive function, and emotion regulation.

The processes of neural development make the brain temporarily more malleable, so that the developing brain can be more vulnerable to insult or more open to positive influences. And because different brain areas have different developmental trajectories, these windows of vulnerability and/or opportunity vary across brain region, as well as across development. Thus, the impact of a stressor or an intervention is likely to quantitatively and/or qualitatively change as a function of developmental timing (Ganzel & Morris, 2011).

Neuro-example #1:The developmental timing of child sexual abuse.

This point is illustrated by a study conducted by Susan Andersen and Martin Teicher from the Harvard Medical School (Andersen et al., 2008). This study used magnetic resonance imaging (MRI) and structural equation modeling to compare regional differences in brain structure in young women who had experienced child sexual abuse (CSA) at different ages, relative to a comparison group that had not experienced CSA.

Women who were abused as preschoolers (between the ages of three and five) showed the greatest reduction in brain volume in a region called the hippocampus, which serves to restrain the hypothalamic-pituitary-adrenal axis (which produces the powerful stress hormone cortisol), as well as playing an important role in the consolidation of long-term memory. These women were also more likely to be currently depressed than women in the comparison group or women who had been abused during any other developmental period.

By contrast, women who had experienced CSA between the ages of nine and ten had smaller volumes of the frontal portion of the corpus callosum, which is the white matter that conveys information between the hemispheres of the brain. These women were more likely to have current symptoms of posttraumatic stress disorder than women in any other group. CSA occurring between the ages of 11 and 13 was again associated with smaller hippocampal volume, but the effect was not as strong as among those women who were abused as preschoolers. Finally, women experiencing child sexual abuse between the ages of 14 and 16 showed reduced volume in prefrontal cortex, which is consistent with ongoing development in this brain area in later adolescence.

This example suggests that developmental timing plays an important role in how (and where) stress might impact the developing brain, with distinctive patterns of long-term consequences for health. There is a large body of research using animal and human models that examines the effect of very early stress on brain, behavior, and health. However, the broader role of developmental timing (i.e., spanning all of development) remains relatively unexplored and may provide important information to guide intervention.

Neuro-example #2: The developmental timing of intervention.

If the developmental timing of stress matters for health outcomes, does the developmental timing of interventions matter, too? We turn to neuroscientific studies of animals to see the direct effects of developmental timing on interventions.

An established body of research has shown that increasing or decreasing the quality of maternal care given to a laboratory rat pup in its first week of life can have permanent consequences for that pup’s cognitive abilities and the neural basis of its stress response (Diorio & Meaney, 2007). This research is often cited in support of interventions that target children ages “zero to three.”

Interestingly, many of the physiological and behavioral deficits associated with low quality early maternal care can be reversed by providing these pups with enriched environments during adolescence (Bredy et al., 2004). Environmental enrichment that occurs earlier or later than adolescence does not have the same beneficial effects. Moreover, enrichment during adolescence also helps to reverse the consequences of other early environmental insults, such as prenatal maternal stress, extended postnatal maternal separation, and early lead exposure. Notably, though, adolescent environmental enrichment does not have an effect on the brains or behavior of pups that had normal early environments and good maternal care. Only the pups at risk benefited from the enrichment intervention during adolescence.

 

These studies suggest the need for considering brain development when determining the type and timing of interventions. Awareness that different brain regions develop according to different timetables may allow us to target our interventions to take best advantage of the natural plasticity inherent in the developing brain.

This is the first of a series of brief articles in which we explore some of the possibilities inherent in these new and broader perspectives on translational neuroscience. We invite you to join us in future articles as we look at how an interdisciplinary perspective that bridges the social and life sciences can inform intervention in support of children and families at risk. In our next installment, we will explore how normal brain maturation has entered the practice and policy arena, such as the 2005 Supreme Court ruling prohibiting death penalty for juveniles. More soon!

 

Dr. Barbara Ganzel, Director, Laboratory for Lifespan Affective Neuroscience
blg4@cornell.edu

 

 

 

References

Andersen, S. L., Tomada, A., Vincow, E. S., Valente, E., Polcari, A., & Teicher, M. H. (2008). Preliminary evidence for sensitive periods in the effect of childhood sexual abuse on regional brain development. Journal of Neuropsychiatry and Clinical Neurosciences, 20, 292–301.

Ansell, E.B., Rando, K., Tuit, K., Guarnaccia, J., & Sinha, R. (2012). Cumulative adversity and smaller gray matter volume in medial prefrontal, anterior cingulate, and insula regions. Biological Psychiatry, 72(1), 57-64.

Bredy, T. W., Zhang, T. Y., Grant, R. J., Diorio, J., & Meaney, M. J. (2004). Peripubertal environmental enrichment reverses the effects of maternal care on hippocampal development and glutamate receptor subunit expression. European Journal of Neuroscience, 20, 1355–1362.

Diorio, J., & Meaney, M. J. (2007). Maternal programming of defensive responses through sustained effects on gene expression. Journal of Psychiatry Neuroscience, 32, 275–284.

Ganzel, B., Kim, P., Glover, G., & Temple, E. (2008). Resilience after 9/11: Multimodal neuroimaging evidence for stress-related change in the healthy adult brain. NeuroImage, 40, 788-795.

Ganzel., B. & Morris, P. (2011). Allostasis and the developing human brain: Explicit consideration of implicit models. Development & Psychopathology, 23, 953-974.

Ganzel, B., Morris, P., & Wethington, E. (2010). Allostasis and the human brain: Integrating models of stress from the social and life sciences. Psychological Review, 117, 134-174.

Gianaros, P. J., Horenstein, J. A., Cohen, S., Matthews, K. A., Brown, S. M., Flory, J. D., . . . Hariri, A. R. (2007). Perigenual anterior cingulate morphology covaries with perceived social standing. Social Cognition and Affective Neuroscience, 2, 161–173.

Gogtay, N., Giedd, J. N., Lusk, L., Hayashi, K. M., Greenstein, D., Vaituzis, A. C., et al. (2004). Dynamic mapping of human cortical development during childhood through early adulthood. Proceedings of the National Academy of Sciences of the United States of America, 101, 8174–8179.

Lane, R. D., & Wager, T. D. (2009). The new field of brain-body medicine: What have we learned and where are we headed? NeuroImage, 47, 1135–1140.

McEwen, B. S. (2007). Physiology and neurobiology of stress and adaptation: Central role of the brain. Physiological Reviews, 87, 873–901.

Taylor, S. E., Eisenberger, N. I., Saxbe, D., Lehman, B. J., & Lieberman, M. D. (2006). Neural responses to emotional stimuli are associated with childhood family stress. Biological Psychiatry, 60, 296–301.

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