Simons Center for the Social Brain

SCSB Lunch Series: Danielle Tomasello, Ph.D.
2019-02-22 12:00 - 13:00 (America/New_York) | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, February 22, 2019
Time: 12:00pm – 1:00pm
Location: Please note the room change — the talk will occur in the McGovern Seminar Room — 46-3189.
Speaker: Danielle Tomasello, Ph.D.
Affiliation: Simons Postdoctoral Fellow, Hazel Sive Laboratory, Whitehead Institute for Biomedical Research.
Talk title: FAM57B Ceramide Synthase, a Hub Gene within 16p11.2 Deletion Syndrome, Maintains Physiological Lipid Membrane Composition
Abstract: The genetic basis for mental health disorders is complex, making diagnostics unreliable and personalized treatments complex. My studies are aimed to address this challenge with a new approach to identify molecular changes in 16p11.2 deletion syndrome. In this prevalent syndrome (occurring in 1 in 2000 individuals) part of chromosome 16 is lost, encompassing a core of 25 genes. Deletion leads to severe brain symptoms including autism, intellectual disability and epilepsy. We hypothesize that the metabolome of neurons is abnormal in individuals with 16p11.2 deletion syndrome, providing a new approach to dissect this complex syndrome. I have concentrated on FAM57B, previously shown to interact with other enzyme-encoded genes within the interval, encoding a ceramide synthase. Consistent with altered metabolism in 16p11.2 deletion syndrome, we see profound changes in lipids in the zebrafish model and in 16p11.2 deletion fibroblasts. fam57b mutants show significant cellular and behavioral phenotypes, including lipid membrane disruption, reduced firing in whole brain recordings and behavioral deficits. We propose FAM57B is a critical protein essential for membrane lipid homeostasis, suggesting haploinsufficiency leads to a cascade of biochemical and cellular changes.

SCSB Colloquium Series - David Ginty, Ph.D.
2019-02-13 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, February 13, 2019
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: David Ginty, Ph.D.
Affiliation: Edward R. and Anne G. Lefler Professor of Neurobiology, Harvard Medical School; Investigator, Howard Hughes Medical Institute.
Talk title: Altered touch processing in neurodevelopmental disorders: mechanisms and emerging therapeutic approaches
Abstract: David Ginty’s laboratory uses mouse molecular genetics, and physiological, anatomical, and behavioral approaches to define: 1) molecular, morphological, and synaptic bases of mammalian mechanosensory neuron subtype properties and functions; 2) the organizational logic of mechanosensory circuits in the spinal cord and brainstem; 3) mechanisms of somatosensory neuron development; and 4) altered mechanosensory neuron reactivity in autism spectrum disorders (ASD) and chronic pain states. This lecture will focus on our work addressing the causes and consequences of mechanosensory circuit dysfunction that underlies aberrant tactile information processing in mouse models of ASD and emergent opportunities for treating tactile over-reactivity.
*** Please note that this talk will not be recorded

SCSB Lunch Series: Nan Li, Ph.D.
2019-02-08 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, February 8, 2019
Time: 12:00pm – 1:00pm
Location: Simons Center Conference Room, Building 46, Room 6011, 6th Floor, MIT (43 Vassar Street, Cambridge, 02139 MA)
Speaker: Nan Li, Ph.D.
Affiliation: Postdoctoral Fellow, Alan Jasanoff Laboratory, MIT
Talk title: Toward functional and molecular neuroimaging analysis of marmoset models
Abstract: Neurodevelopmental disorders affect many aspects of brain function, and surveying phenotypic abnormalities across altered brains can be challenging. Our group has created a suite of novel tools that can probe molecular-level hallmarks of brain function by magnetic resonance imaging (MRI), potentially enabling qualitatively new and mechanistically informative approaches to the analysis of brain-wide dysfunction in autism and other conditions. Here I will present our recently developed molecular imaging approaches for mapping spatiotemporal dynamics of diverse neural signaling components, including dopamine release and calcium signaling. Initial application of these tools has taken place in rodents, but we expect our molecular imaging methods to be of outstanding utility for whole-brain functional analysis of emerging primate disease models. I discuss progress toward establishing fMRI in awake marmosets at MIT, with the future goal of applying novel functional and molecular imaging techniques to characterize marmoset models of autism spectrum disorders.

SCSB Lunch Series: Guoping Feng, Ph.D.
2018-12-14 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, December 14, 2018
Time: 12:00pm – 1:00pm
Location: Simons Center Conference Room, Building 46, Room 6011, 6th Floor, MIT (43 Vassar Street, Cambridge, 02139 MA)
Speaker: Guoping Feng, Ph.D.
Affiliation: Poitras Chair Professor of Neuroscience, McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, MIT; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard.
Talk title: Thalamic reticular nucleus dysfunction in neurodevelopmental disorders
Abstract: The Thalamic reticular nucleus (TRN) provides major inhibitory inputs to the thalamus and plays important roles in sensory gating, attention selection and sleep rhythms. Many of the risk genes for ASD, schizophrenia and ADHD are highly expressed in the TRN, raising the possibility that TRN may be a circuit converging point for some of the overlapping behavioral abnormalities in these disorders. Using TRN-specific genetic deletions in mice, we demonstrate the critical roles of TRN dysfunction in attention deficit, hyperactivity and sleep disruption, commonly observed in neurodevelopmental disorders including ASD. Using multi-scale single cell analysis including single cell RNA-Seq, multiplex RNA FISH, electrophysiological recordings and molecular tracing. We identified two major TRN neuronal subtypes that have distinct electrophysiological properties, differential topographic connectivity related to different thalamic sensory modalities, i.e. first order and high order thalamic nuclei. Through such non-overlapping anatomical pathways mediated by its subpopulations, TRN might differentially tune incoming sensory information through thalamo-cortical circuits. Importantly, we identified genes selectively expressed by each of the TRN subtypes of neurons, paving the way for testing molecular targets that could potentially regulate different TRN functions based on their thalamic connectivity.

SCSB Colloquium Series: Nathalie van Bockstaele
2018-12-05 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Artwork created by Clovis
A show and tell about ♫ (sound bite)
Autism, Interdependence and Reciprocity
Presenters:
Nathalie van Bockstaele | Concept designer and performer
Jason O’Keefe, Elise L’Herault, Michael Jauquet, Noa Alon | Artist performers
Pablo Friedmann | Fellow artist, mentor and partner
Jocelyn Odóna Holm, Jackie Lee | Discussants
* Click here for presenter bios
Host: Mriganka Sur, Ph.D., FRS
Abstract:
We, parent, companions, and friends, present our real life experience with autism and what we have learned from it: how practicing increased dependence makes us aware of interdependence; how positing reciprocity (which in a quasi-nonverbal environment amounts to observing actions and responding to them) opens original dialogues; and how, as a result, interacting with autism promotes constant creativity in order to both decipher and offer feedback.
What you are going to see are demonstrations in the form of gestures we have shaped from our experience. We urge you to imagine—that is to actively build in your mind a representation of what underlies our choice of gestures—what they stand for and reveal and how you would respond. We address these concepts multiple times, with the help of our discussants, before we open the Q&A exchange.
[Video of the talk]

Date: Wednesday, December 5, 2018
Time: 4:00 pm-5:00 pm, followed by reception
Location: MIT Building 46-3002 (Singleton Auditorium), 3rd Floor, 43 Vassar Street, Cambridge, MA 02139
Please click here to register for this event: https://www.eventbrite.com/e/scsb-colloquium-series-nathalie-van-bockstaele-tickets-52418493124
*** Please note that a legal ID (Driver’s License, Passport, etc.) is required for alcoholic beverages at the reception.

SCSB Colloquium Series - Ilana Witten, Ph.D.
2018-11-28 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, November 28, 2018
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Ilana Witten, Ph.D.
Affiliation: Associate Professor, Neuroscience Institute & Department of Psychology, Princeton University
Host: Ann Graybiel, Ph.D.
Talk title: Prefrontal-striatal interactions in social learning, and beyond
Abstract: In the part of my talk, I will present our recent work examining the role of prefrontal neurons that project to the nucleus accumbens in social learning. I will also show some new data on how these neurons may represent social stimuli differently from other prefrontal neural populations. In the second part of my talk, I will present unpublished data on the role of prefrontal neurons that project to the nucleus accumbens in drug seeking, and examine how their properties change in animals with greater drug motivation.
*This talk will not be video recorded.

SCSB Lunch Series: Rogier Landman, Ph.D.
2018-11-16 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, November 16, 2018
Time: 12:00pm – 1:00pm
Location: Simons Center Conference Room, Building 46, Room 6011, 6th Floor, MIT (43 Vassar Street, Cambridge, 02139 MA)
Speaker: Rogier Landman, Ph.D.
Affiliation: Research Affiliate, McGovern Institute for Brain Research, MIT
Talk title: Behavioral characterization of non-human primates for autism research
Abstract: Disruption of the Shank3 gene has been implicated as a monogenic cause of Autism Spectrum Disorders. Although rare in humans, understanding how this mutation leads to symptoms could ultimately reveal how genetic factors in general affect the likelihood of autism. I will talk about behavior of a small group of CRISPR/Cas9 generated Shank3 mutant macaque monkeys using behavior scoring, eye tracking, movement tracking and social interaction. To analyze future genetic models in the common marmoset we have developed assays including eye tracking, automated movement and vocalization tracking, infant neurobehavioral screening, in-cage training and awake fMRI training.
Bio: Rogier Landman got his PhD at the University of Amsterdam, The Netherlands. He has investigated the neuronal mechanisms of visual attention and the influence of social stimuli on attentional capture. His current work involves automated behavioral monitoring and analysis of macaque and marmoset monkeys in the context of autism and schizophrenia.

SCSB Colloquium Series - Elise Robinson, Ph.D.
2018-11-14 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, November 14, 2018
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Elise Robinson, Ph.D.
Affiliation: Assistant Professor, Department of Epidemiology, Harvard TH Chan School of Public Health; Associate Member, Broad Institute
Host: Mriganka Sur, Ph.D., FRS
Talk title: Autism heterogeneity: genetic insights and next steps.
Abstract: ASD researchers have long been aware that two people with a diagnosis of autism can be as different from one another as two people in any classroom or neighborhood. Translating that awareness into the design of research studies, however, has often presented a challenge. Over the last five years, genetic studies have produced a wealth of unambiguous associations to ASD risk, and taught us that genetic heterogeneity in ASD is patterned. Dr. Robinson will provide an introduction to ASD genetics and discuss how knowledge of genetic heterogeneity can inform research targeting ASD biology.

SCSB Special Seminar - Francisco Clascá, MD, PhD.
2018-11-09 11:00 - 12:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Friday, November 9, 2018
Time: 11:00 am – 12:00 pm
Speaker: Francisco Clascá, M.D., Ph.D.
Affiliation: Professor of Human Anatomy & Neuroscience, Dept. of Anatomy & Graduate Program in Neuroscience; Director, Applied Anatomy Center, Autónoma de Madrid University, School of Medicine
Hosts: Michael Halassa, Ph.D., Mriganka Sur, Ph.D., FRS
Talk title: Wiring for cognition: axonal and synaptic diversity of thalamocortical higher-order pathways.
Abstract: I will review recent evidence that the circuits created by thalamic projection neuron axons are far more complex and synaptically diverse than previously believed. Through branched axons and diverse synaptic structures, individual thalamic neurons may selectively share signals, according to behaviorally-relevant logic, with several cortical and subcortical cell populations.

Bio: I hold an M.D. from The Basque Country University, Bilbao, Spain (1983), and a Ph.D. in Neuroscience from the Autonoma University of Madrid (1990).
In my PhD Thesis I defined the cat’s insular cortex based on thalamic and cortical connectivity. After a postdoctoral training in the lab of Carlos Avendaño, also in Madrid, working on claustro-cortical circuitry (1990-92), I joined Mriganka Sur’s laboratory at the Dept. of Brain & Cognitive Sciences at MIT (1992-95). There, I investigated the developmental plasticity of axonal pathways between thalamus and cortex in carnivores. After returning to Spain, I set up an independent lab at the Autonoma University of Madrid, and examined the timing and molecular signals involved in the development of thalamocortical pathways.
My research project is elucidating, with single-cell resolution, the network architectures created by the projection neuron populations that interconnect the cortex and thalamus. My lab’s work is at present focused on the axonal and synaptic diversity of the thalamocortical neurons in rodent and primate models. We apply population and single-cell neuronal tracing and quantitative analysis methods at the optical and EM level and extracellular and intracellular recording techniques.

SCSB Colloquium Series - Elizabeth Redcay, Ph.D.
2018-10-24 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, October 24, 2018
Time: 4:00 pm-5:00 pm
Speaker: Elizabeth Redcay, Ph.D.
Affiliation: Associate Professor of Psychology, University of Maryland
Host: Rebecca Saxe, Ph.D.
Talk title: A social-interactive neuroscience approach to understanding autism.
Abstract: Difficulty with reciprocal social interaction is a core diagnostic feature of autism spectrum disorders (ASD) but the specific neural systems underlying these difficulties remain unclear. Dominant theories suggest a role for social-motivational and social-cognitive brain networks; however, these theories have been tested primarily using non-interactive (“offline”) tasks in which participants are not engaged in social interaction. In this talk, I argue that this “offline” approach presents a barrier to our understanding of the neural mechanisms underlying social interaction in autism. Through a series of studies, I demonstrate that social-interactive context changes the way social stimuli are processed. Specifically, the perception of an online social partner leads to spontaneous recruitment of the brain’s mentalizing network even without explicit demands to reason about the partner’s mental state (or “mentalize”). I then discuss current work using a social-interactive (“online”) approach to examine the role of social-cognitive and social-motivational brain networks in social interaction in typically developing and ASD children.
[Video of the talk is available upon request: asokhina@mit.edu]

SCSB Lunch Series: Jakob Voigts, Ph.D.
2018-10-19 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, October 19, 2018
Time: 12:00pm – 1:00pm
Location: Simons Center Conference Room, Building 46, Room 6011, 6th Floor, MIT (43 Vassar Street, Cambridge, 02139 MA)
Speaker: Jakob Voigts, Ph.D.
Affiliation: Simons Fellow, Mark Harnett Lab, MIT
Talk title: Dendritic mechanisms for navigation in retrosplenial cortex
Abstract: Navigation requires associating different streams of information. For example, recognizing a distant skyscraper while facing north vs. facing south has different interpretations for one’s position. Retrosplenial cortex, thought to be the main hub for carrying out such associations during navigation, is well suited to testing how individual neurons can flexibly combine multiple inputs to implement such computations. I will present results using recently developed technology that allows us to combine, for the first time, 2-D navigation with head rotation and conventional 2-photon imaging of dendrites. My findings show that dendritic activity is less modulated by context than the somatic outputs of neurons, suggesting that head-direction input is processed by active dendritic mechanisms. I will discuss how this approach can be used to study the link between within-neuron and network computations in general associative cortical computations.

SCSB Colloquium Series - John Huguenard, Ph.D.
2018-10-10 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, October 10, 2018
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: John Huguenard, Ph.D.
Affiliation: Professor of Neurology and Neurological Sciences, Neurosurgery, and Molecular and Cellular Physiology, Stanford University School of Medicine

Host: Guoping Feng, Ph.D.
Talk title: Loss of axonal function in maternal immune activation models of autism spectrum disorders.
Abstract: Autism spectrum disorder (ASD) is a complex heterogeneous neurodevelopmental syndrome with genetic and environmental risk factors. Infection during pregnancy is strongly implicated as an environmental factor, with maternal immune activation (MIA) identified in the causative pathway. However, a mechanistic understanding of MIA-induced alterations in brain function and accompanying social behavior remains elusive. Here, using an established MIA mouse model, we find that offspring exhibit a profound and persistent impairment in excitability of the medial prefrontal cortex (mPFC) – a major locus of social cognition and ASD pathology. Specifically, we report novel disorganization of the axon initial segment and blunted transmission along the distal axon. Transcriptomic analysis identified L1cam deficiency as a likely key mediator of these structural and functional impairments. Downregulation of L1cam in mPFC was found to reproduce sociability deficits. These results demonstrate a novel mode of circuit dysfunction in ASD – disrupted axonal signaling – which fundamentally alters the output of mPFC neurons.
[Video of the talk]

SCSB Lunch Series: Yang Zhou, Ph.D.
2018-10-05 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, October 5, 2018
Time: 12:00pm – 1:00pm
Location: Simons Center Conference Room, Building 46, Room 6011, 6th Floor, MIT (43 Vassar Street, Cambridge, 02139 MA)
Speaker: Yang Zhou, Ph.D.
Affiliation: Research Scientist, Guoping Feng Lab, McGovern Institute for Brain Research, MIT
Talk title: Searching the Neural Basis of ASD from Genetically Engineered Model Systems
Abstract: Progress in understanding the neural basis of ASD is inspiring yet unsubstantial over the past decade, in part due to the lack of reliable model systems. Recapitulating core cognitive and behavioral dysfunctions which are closer and relevant to affected human individuals represents one of the significant challenges. Deletion or point mutation of synaptic genes, such as SHANK3 are frequently identified from idiopathic human ASD, allowing for the creation of engineered model systems with which to uncover the molecular, cellular pathophysiology and decipher the neural signature underlying ASD. I will report our efforts in developing advanced ASD models using cutting-edge genetic technologies and discuss behavioral as well as neural circuit alterations identified from models with the Shank3 mutation. We anticipate that our research will provide a critical step forward in the discovery of translatable biomarkers, as well as developing and testing of therapeutic strategies for ASD.

SCSB Colloquium Series - Alika Maunakea, Ph.D.
2018-09-26 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, September 26, 2018
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Alika Maunakea, Ph.D.
Affiliation: Associate Professor, Epigenomics Research Program, Department of Native Hawaiian Health, John A. Burns School of Medicine, University of Hawai’i, Mānoa
Host: Ravikiran Raju, M.D., Ph.D.
Talk title: Integrative epigenomic analyses support the early developmental origin of autism spectrum disorders.
Abstract: Autism spectrum disorders (ASD) are clinically heterogeneous neurobehavioral diseases suspected to originate in utero when brain cells undergo widespread epigenetic changes to the underlying chromatin landscape, including DNA methylation. Although the normal trajectory of DNA methylation is thought to be critical to transcriptional regulation in neurodevelopment, whether it is compromised in ASD is unknown. Using two complementary genome-wide approaches, we observed significant alterations to DNA methylation in a neural stem cell compartment of postmortem brain from individuals diagnosed with ASD. We found that many of these ASD-specific alterations reside within developmentally regulated chromatin domains, the methylation states of which remarkably resembled that of early fetal brain. Transcriptomic analyses independently demonstrated fetal stage-specific gene expression states in these affected individuals. Together, these findings suggest ASD may arise as a consequence of an “epigenetic delay” in shaping the chromatin landscape during neurodevelopment, providing molecular support of pathological observations implicating its early fetal origins.
[Video of the talk]
Biography:
Dr. Maunakea received his B.Sc. degree in Biology at Creighton University (2001) and Ph.D. in Biomedical Sciences at the University of California, San Francisco (2008). He completed Postdoctoral training at the National Institutes of Health (2012) and has since joined the John A. Burns School of Medicine at the University of Hawaiʻi, Mānoa. In studying epigenetics for over 15 years, Dr. Maunakea has made several important contributions that have helped advance the field. In particular, he has developed and applied novel high-throughput, genome-wide technologies that survey DNA methylation and histone modifications (Ching et al., 2005; Corley, Zhang, Zheng, Lum-Jones, & Maunakea, 2015; Kraushaar et al., 2013), both central components of epigenetic processes, and has discovered novel roles for DNA methylation in regulating alternative promoter usage (Maunakea, Nagarajan, et al., 2010) and in pre-mRNA splicing (Maunakea, Chepelev, Cui, & Zhao, 2013). In his current position as Associate Professor in the Department of Native Hawaiian Health, Dr. Maunakea is applying epigenomic information toward understanding the mechanistic relationships of gene-environment interactions that underlie the development of diseases of health disparities, including autism and cardiometabolic diseases, anticipating that such studies will contribute to the development of more effective targeted diagnostic, preventative, and therapeutic strategies.

SCSB Lunch Series: Laurel Gabard-Durnam, Ph.D.
2018-09-14 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, September 14, 2018
Time: 12:00pm – 1:00pm
Location: Simons Center Conference Room, Building 46, Room 6011, 6th Floor, MIT (43 Vassar Street, Cambridge, 02139 MA)
Speaker: Laurel Gabard-Durnam, Ph.D.
Affiliation: Autism Science Foundation Postdoctoral Fellow, Labs of Cognitive Neuroscience, Boston Children’s Hospital, Harvard Medical School
Talk title: “Neuroimaging evidence for Autism biomarkers across the first year of life”
Abstract: An outstanding issue in Autism Spectrum Disorder (ASD) research is the identification of biomarkers to expedite detection and provide insight into pathophysiology. The search for early neuroimaging biomarkers is both promising and challenging as they occur before behavioral symptoms emerge but during extensive changes in brain function. I will present evidence from 2 longitudinal EEG studies in infants at low- and high-familial risk for ASD that leverage neurodevelopmental changes to identify early biomarkers. These studies show that EEG within the first year of life differentiates infants with future ASD diagnoses, and they provide a mechanism through which disrupted neuroplasticity contributes to ASD. Together, these findings speak to the potential of early EEG-based biomarkers for identifying and understanding neurodevelopmental trajectories in ASD.

SCSB Colloquium Series - Jaideep Bains, Ph.D.
2018-09-12 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, September 12, 2018
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Jaideep Bains, Ph.D.
Affiliation: Professor, Hotchkiss Brain Institute, University of Calgary
Host: Kay Tye, Ph.D.
Talk title: Social Transmission of Stress.
Abstract: Stress can trigger enduring changes in neural circuits and synapses. Recent findings from our lab show that mice rely on social interactions with others to transmit and extract odor features that transmit and buffer the effects of stress (Sterley et al, Nat Nsci, 2018). The synaptic consequences of transmitted stress on are not distinguishable from authentic stress. Intriguingly, social interactions with unstressed individuals buffer the effects of stress, but only in female subjects. Finally, we show that stress-induced synaptic changes can be transmitted sequentially from the stressed subject to multiple partners. Our findings demonstrate that transmitted stress has the same lasting effects on glutamate synapses as authentic stress and reveal an unexpected role for PVN CRH neurons in transmitting distress signals among individuals.
[Video of the talk]

SCSB Lunch Series: Jeong-Tae Kwon, Ph.D.
2018-06-01 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, June 1, 2018
Time: 12:00pm – 1:00pm
Location: Simons Center Conference Room, Building 46, Room 6011, 6th Floor, MIT (43 Vassar Street, Cambridge, 02139 MA)

Speaker: Jeong-Tae Kwon, Ph.D.
Affiliation: Simons Postdoctoral Fellow, Gloria Choi Laboratory, McGovern Institute for Brain Research, MIT
Talk Title: “Neuromodulatory Control of Social Behavior in Amygdala”
Abstract: Innate social behaviors, such as reproduction and aggression, need to be tightly regulated to prevent inappropriate social interactions under adverse conditions. While previous studies have mostly focused on the induction of innate social behaviors, neural circuits and mechanism, by which these behaviors are inhibited under inappropriate conditions, are poorly understood. I will present our recent finding that the posteromedial cortical amygdala plays a key role in suppression of social behaviors, such as mounting and attacking, in the adverse conditions (e.g. infectious conspecifics or unfamiliar place). Our results suggest that the suppression effect is mediated through thyrotropin-releasing hormone (TRH) signaling in intra-amygdala circuits. Together, these findings will provide a new understanding into how neuromodulatory signaling in the amygdala guides relevant behavioral outputs that are based on the conditions an individual encounters.

SCSB Colloquium Series - Eric J. Nestler, M.D., Ph.D.
2018-05-16 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, May 16, 2018
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Eric J. Nestler, M.D., Ph.D.
Affiliation: Nash Family Professor of Neuroscience; Director, Friedman Brain Institute; Dean for Academic and Scientific Affairs, Icahn School of Medicine at Mount Sinai
Host: Yingxi Lin, Ph.D.
Talk title: Transcriptional and Epigenetic Mechanisms of Depression.
Abstract: Depression is a common, chronic, and debilitating disease. Although many patients benefit from antidepressant medications or other therapies, only about half of depressed patients show a complete remission, which underscores the need for more effective agents. The mechanisms that precipitate depression, such as stress, are incompletely understood. One mystery of the disease is its long-lasting nature and delayed response to antidepressant treatment. This persistence is thought to be mediated by slowly developing but stable adaptations in the brain, which might include regulation of gene expression and chromatin structure.
We have used several chronic stress procedures in mice, such as chronic social defeat stress and chronic variable stress, as models of depression that mimic key symptoms seen in humans. An important feature of this work is to examine not only those mice that succumb to the stress (susceptibility), but also those that avoid deleterious outcomes (resilience). We are exploring the molecular basis of stress-induced behavioral pathology, antidepressant action, and resilience by analyzing genome-wide changes in gene expression and chromatin modifications in several limbic brain structures. Parallel work has focused on homologous regions in the brains of depressed humans examined postmortem. We are using these datasets to understand prominent sex differences in stress responses in mice and depression in humans as well as to identify the mechanisms by which early life experience controls stress vulnerability for a lifetime.
Together, this work is providing novel insight into the molecular mechanisms underlying depression and other stress-related disorders. The findings also suggest novel leads for the development of new antidepressant treatments. For example, our findings on resilience suggest the novel approach of developing medications that promote resilience and not just those that oppose the deleterious effects of stress.
[Video of the talk]

SCSB Lunch Series: Sasha Krol, Ph.D.
2018-05-04 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, May 4, 2018
Time: 12:00pm – 1:00pm
Location: Simons Center Conference Room, Building 46, Room 6011, 6th Floor, MIT (43 Vassar Street, Cambridge, 02139 MA)
Speaker: Sasha Krol, Ph.D.
Affiliation: Simons Fellow, Feng Lab, McGovern Institute, MIT
Talk Title: “Uncovering the developmental and circuit origin of ASD-associated aggression”
Abstract: In addition to core symptoms including social deficits and repetitive behaviors, individuals with autism spectrum disorder (ASD) experience many other debilitating symptoms including aggression, an extremely challenging social disruption. Although dysfunction of hypothalamic circuitry has long been appreciated to be a key mediator of aggression in animal studies, increased aggression in the context of ASD is poorly understood due to a lack of good models. To address this gap, we are using a neurodevelopmental/ASD mouse model of human patients with deletion of PTCHD1, a condition that contributes to ~1% of ASD cases with intellectual disability (ID) and leads to hyper-aggression, a behavior which is recapitulated in the Ptchd1 mutant mouse. Using this model we are determining the circuitry responsible for Ptchd1- mediated, ASD-related aggression. Additionally we are dissecting the temporal requirement of Ptchd1 in the development of aggressive behavior. Together our results will identify a target circuit and temporal window for designing and testing therapies for aggression in ASD and other disorders.

SCSB Lunch Series: Julian Jara-Ettinger, Ph.D.
2018-04-27 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, April 27, 2018
Time: 12:00pm – 1:00pm
Location: Simons Center Conference Room, Building 46, Room 6011, 6th Floor, MIT (43 Vassar Street, Cambridge, 02139 MA)
Speaker: Julian Jara-Ettinger, Ph.D.
Affiliation: Assistant Professor of Psychology and Computer Science, Yale University
Talk Title: “Computational principles underlying social cognition: similarities and differences in ASD”
Abstract: Autistic Spectrum Disorders are diagnosed partly on the basis of impairments in social cognition. However, understanding the exact nature of these deficits has been difficult because there is no characterization of the nature of social inferences in typical development. In this talk I will present a theory of social cognition that posits a naïve utility calculus as the engine for making sense of the social world. I will show that even young children rely on this naïve utility calculus when they interpret other people’s actions, when they make moral evaluations, and when they interpret what other people say. Next, I will present a formal computational model that predicts with quantitative accuracy how neurotypical adults reason about simple social events, and I will show how, by using this model, we can uncover fine-grained similarities and differences in autistic adults.

SCSB Colloquium Series - Ania Majewska, Ph.D.
2018-04-18 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, April 18, 2018
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Ania Majewska, Ph.D.
Affiliation: Associate Professor, Department of Neuroscience, University of Rochester
Host: Mriganka Sur, Ph.D., FRS
Talk title: Microglia and synapses: partners in experience-dependent plasticity
Abstract: The ability to tune synapses, and thus alter neural networks, is critical to both the normal development of brain circuitry and brain function throughout life, underlying processes such as learning and memory. Microglia are immune cells that infiltrate the brain early in development before the formation of the blood brain barrier. They have critical roles during brain injury, infection or disease. However, new data has thrust these non-neural cells into the spotlight as regulators of synapses. In the absence of pathology, microglia display dynamic interactions with synapses, and contribute to experience-dependent plasticity in the visual cortex in vivo. Manipulations of visual experience elicit a remarkably rapid behavioral response in microglia which is distinct from their inflammatory response, and includes an increase in phagocytosis that corresponds to the early phase of plasticity when synapses are lost in this model and when microglia increase their synaptic interactions. Our recent work has focused on identifying the molecular mechanisms through which microglia respond to changes in neuronal activity and communicate with synapses. I will also discuss our work exploring the contribution of these cells to plasticity deficits observed in a mouse model of third trimester alcohol exposure. Together, our findings suggest that microglia play an important role in synaptic plasticity, and use a subset of their pathological molecular repertoire to implement plastic changes in the non-pathological brain.
[Video of the talk]

SCSB Lunch Series: Caroline Robertson, Ph.D.
2018-04-06 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, April 6, 2018
Time: 12:00pm – 1:00pm
Speaker: Caroline Robertson, Ph.D.
Affiliation: Postdoctoral Fellow, MIT McGovern Institute, Incoming Assistant Professor, Dartmouth College
Talk Title: “Advancing a Marker of Reduced GABAergic Action in the Autistic Brain: Pharmacological Investigations”
Abstract: We have recently developed a robust and replicated behavioral marker of autism in visual perception — reduced perceptual suppression during binocular rivalry (Robertson et al., 2013, JNeuro) — which links to the reduced action of the inhibitory neurotransmitter γ-aminobutyric acid (GABA) in the autistic brain (Robertson et al., 2016, Current Biology).
Our current work aims to develop this marker as tool to facilitate animal and genetic research and pharmacological interventions in the condition. Towards this end, here we tested a causal link between the strength of perceptual suppression during rivalry and the inhibitory neurotransmitter, GABA, using pharmacological manipulations.
22 healthy adults participated in each of three separate studies, investigating the effects of a GABAA modulator (Clobazam; study 1), a GABAB modulator (Arbaclofen; study 2), and a Cl- channel modulator (Bumex; study 3) on binocular rivalry dynamics. Each study took place over 3 days, in a counter-balanced double-blind design. On each of the experimental days, a participant was given either a drug or a placebo, and participated in a short binocular rivalry experiment after the drug had come into effect. Each GABAergic modulator exerted a strong effect and specific effect on perceptual suppression during rivalry. Importantly, binocular rivalry dynamics were highly test-retest reliable across testing days (all Rho > 0.65, all p < 0.001), and measures of drowsiness did not influence key results.
These findings provide a causal, mechanistic link between the GABA pathway and perceptual suppression, as suggested by our previous Magnetic Resonance Spectroscopy research and computational models of rivalry. These results also identify specific aspects of the GABAergic pathway which are involved in supporting binocular rivalry. All in all, our results flag perceptual suppression as a marker of GABAergic drug response.

SCSB Colloquium Series - Peggy Mason, Ph.D.
2018-03-28 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, March 28, 2018
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Peggy Mason, Ph.D.
Affiliation: Professor, Department of Neurobiology, University of Chicago
Host: Mriganka Sur, Ph.D., FRS
Talk title: The Neurobiology of Helping: Lessons from Order Rodentia
Abstract: Among mammals, social interactions are critical for survival of the individual and the species. Moreover, by facilitating safety, food procurement, shelter and well-being, sociality also allows for longer, more rewarding lives. Pro-social behavior, or helping, that is provided between members of a group increases social cohesion of that group. Given the evolutionary advantages of pro-social behavior, it is not surprising that rats help other rats just as primates, including humans, do. Recently, my laboratory has demonstrated that rats deliberately liberate a conspecific trapped within a restrainer. Helping persists even when the free rat is unable to physically interact with the liberated rat. Moreover, helping is socially selective, occurring only for rats of a familiar type but independent of individual familiarity.
A key question is the motivation that drives rats to help another in distress. We have demonstrated that some degree of affective distress within the helper is required for motivating helping. Yet, to our surprise, helper rats help even when the victim rat shows no distress, evidence that cognitive empathy can motivate a rat witness to action. An additional motivating factor for helping is a rat’s assessment of other rats’ assessments of the trapped rat. Reminiscent of the human bystander effect, rats are more likely to help in the presence of naïve rats and less likely to help in the presence of non-helper (confederate) rats. In sum, the conservation of complex motivated helping behavior across divergent mammals raises the exciting possibility that we can learn about the social influences on human mood from rat experiments.
[Video of the talk]

SCSB Lunch Series: Siyuan Rao, Ph.D.
2018-03-23 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, March 23, 2018
Time: 12:00pm – 1:00pm
Speaker: Siyuan Rao, Ph.D.
Affiliation: Polina Anikeeva Laboratory, Research Laboratory of Electronics and Simons Center for Social Brain, MIT
Talk Title: Magnetochemogenetic Technique for Remote Manipulation of Genetically Identifiable Neurons
Abstract: For the rodent models of Autism Spectrum Disorders, whose behavior is sensitive to the implanted foreign objects, investigation of the neural circuits underlying their abnormal behavioral phenotypes via invasive optogenetic and electrical neuromodulation devices poses a challenge. Here we developed a minimally invasive neuromodulation tool for magnetothermal deep brain interrogation of genetically identifiable neural populations in freely moving rodents. This approach enabled temporally and spatially precise chemical manipulation of neural activity by local release of designer drugs in response to remote exposure to alternating magnetic fields. We achieved the implant-free convenience of magnetothermal neuromodulation concomitantly with the genetic precision of chemogenetics, and thus enabled spatial and temporal modulation for behavioral investigation. We anticipate that the magnetochemogenetic tools will facilitate investigation of neural circuits during behavioral experiments and enable neuromodulation studies in rodent models incompatible with permanently implanted hardware.

SCSB Colloquium Series - Randall Carpenter, M.D.
2018-03-21 10:00 - 11:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Randall Carpenter, MD, Co-Founder, President and CEO Seaside Therapeutics..photo by www.mckeephotography.com..For use and publication by Seaside Therapeutic and editorial publications…For more information about the photograph, mckeephotography.com, matt@mckeephotography.com.617-910-9314
Wednesday, March 21, 2018
Time: 4:00 pm-5:00 pm, followed by reception . NEW TIME: 10:00 am-11:00 am
Speaker: Randall L. Carpenter, M.D.
Affiliation: Chief Scientific Officer, Rett Syndrome Research Trust; Research Affiliate, Picower Institute for Learning and Memory
Host: Mark Bear, Ph.D.
Talk title: Development of Targeted Therapeutics for Autism Spectrum Disorders.
Abstract: Twelve years ago, I co-founded Seaside Therapeutics ​with an MIT professor based upon a strong sense of optimism that substantial progress would soon be realized in treatment of neurodevelopmental disorders. A new era of molecular genetics and neurobiology suggested that genetic diagnoses need not equate to permanent mental disability, but can actually provide insights toward disease-altering treatments. A number of highly penetrant genetic mutations had been discovered and reproduced in animal models. ​novel therapeutics targeting the underlying pathophysiology were ​being ​validated in these animal models and preliminary human trials ​were demonstrat​ing​ promising efficacy. However, ​subsequent larger definitive trials failed to demonstrate convincing therapeutic benefit. This lecture will address how these failures are informing therapeutic discovery and development with a particular focus on ​the ​R​ett S​yndrome ​R​esearch ​T​rust​’s ​R​oadmap ​to a Cure for Rett Syndrome. ​
[Video of the talk]

SCSB Colloquium Series - Joshua Kaplan, Ph.D.
2018-02-21 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, February 21, 2018
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Joshua Kaplan, Ph.D.
Affiliation: Professor of Neurobiology, MGH/Harvard Medical School
Host: Steven Flavell, Ph.D.
Talk title: From compost to the clinic: using C. elegans to study psychiatric disorders.
Abstract: Recent human genetic studies suggest that mutations in ~500 genes are linked to autism spectrum disorder. Although many of these genes encode proteins that are localized at synapses, relatively little is known about how these mutations alter brain function or development. An important goal for the field is to identify specific cellular defects caused by mutations linked to Autism and to determine how (and if) these defects contribute to the cognitive and developmental deficits found in Autism. My lab uses a simple model organism (Caenorhabditis elegans) as a genetic platform to investigate the impact of Autism-linked genes on brain development and function. C. elegans is a small worm (1 mm long as an adult) that lives in rotting organic matter (like compost heaps).
Our studies suggest that mutations linked to Autism in humans alter retrograde synaptic signals, the strength of inhibitory synapses, and activity-induced gene expression in worms. We propose that these cellular defects play an important role in the pathophysiology of Autism.

SCSB Lunch Series: Dara Manoach, Ph.D.
2018-02-16 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, February 16, 2018
Time: 12:00pm – 1:00pm
Speaker: Dara S. Manoach, Ph.D.
Affiliation: Professor of Psychology, Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School
Talk Title: Abnormal sleep spindles in neurodevelopmental disorders: Treatable endophenotypes that link risk genes to impaired cognition?
Abstract: Although neurodevelopmental disorders are defined by waking phenomena, abnormal sleep is a pervasive feature that may contribute to their manifestations. In schizophrenia, there is convincing evidence that sleep spindle deficits impair memory consolidation. Sleep spindles, a defining EEG oscillation of Stage 2 sleep, are initiated in the thalamic reticular nucleus and are a product of thalamocortical interactions. I will review evidence that spindle deficits in schizophrenia are: (i) genetically-mediated, (ii) associated with abnormal thalamocortical interactions, (iii) impair sleep-dependent memory consolidation, (iv) contribute to symptoms and (v) are a novel treatment biomarker. I will end by describing our collaborative study of sleep spindles in autism.
Dara Manoach is a Professor of Psychology in the Department of Psychiatry at Massachusetts General Hospital and Harvard Medical School. She is a neuropsychologist whose research program uses multimodal neuroimaging to illuminate the neural bases of cognitive deficits in neuropsychiatric and neurodevelopmental disorders, particularly schizophrenia and autism. The ultimate goal of this work is to identify mechanisms of cognitive impairment that can guide the development of treatment. Her primary area of research focuses on the contribution of abnormal sleep to memory consolidation deficits. Dr. Manoach received her doctorate from Harvard University in Experimental Psychology, completed a clinical psychology internship at McLean Hospital and a postdoctoral fellowship in clinical neuropsychology at Beth Israel Hospital of Harvard Medical School. At MGH she directs the Laboratory for Multimodal Neuroimaging of Cognition in Psychopathology (Manoach Lab) at the Athinoula A. Martinos Center for Biomedical Imaging.

SCSB Lunch Series: Ted Gibson, Ph.D.
2018-02-09 12:00 - 13:00
Date: Friday, February 9, 2018
Time: 12:00pm – 1:00pm
Speaker: Ted Gibson, Ph.D.
Affiliation: Professor of Cognitive Science, Department of Brain & Cognitive Sciences, MIT
Talk Title: The structure of pragmatic reasoning and the scope of the communicative impairment in ASD.
Abstract: Language comprehension entails more than simply decoding the literal meaning of an utterance: our interpretation is powerfully shaped by the perceived intent of the speaker, the linguistic and social context of the utterance, and our general world knowledge. This ability to exploit speaker intent and background knowledge to go beyond the literal meaning is referred to as “pragmatics”, and is at the core of communicative success. The term “pragmatics”, as used in the literature, encompasses a wide range of diverse phenomena, from irony and sarcasm, to understanding scalar implicatures, to using prosodic cues, to making world-knowledge-based inferences. In an ongoing project, we are using an individual-differences approach to investigate the structure of mental processes relevant to pragmatic reasoning. To do this, we developed an extensive battery consisting of 20 tasks that tap 11 distinct phenomena. Across a large sample of neurotypical adults (n=~400) tested on Mechanical Turk, factoring out IQ, we discovered a remarkably clear clustering of tasks into sensible categories. The biggest category included phenomena that appear to involve higher-order expectations about social norms, like irony, white lies, and humor. Other categories included world-knowledge-based inferences, prosodic processing, and understanding scalar implicatures. We then asked which of these components of pragmatic reasoning are impaired in individuals with ASD. In a sample of 18 participants (data collection ongoing), we found impairments in a) the component that deals with higher-order expectations about social norms, and b) world-knowledge-based inferences, but not in prosodic processing or understanding scalar implicatures. Thus, we are making some progress in both carving up the mental architecture of pragmatic processing, and trying to delineate the scope of the communicative impairment in ASD.

SCSB Colloquium Series - Lauren Atlas, Ph.D.
2018-01-24 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, January 24, 2018
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Lauren Atlas, Ph.D.
Affiliation: Clinical Investigator / Section Chief, National Institutes of Health (National Center for Complementary and Integrative Health, National Institutes on Drug Abuse)
Host: Ev Fedorenko, Ph.D.
Talk title: How instructions, expectations, and conditioning modulate pain and aversive learning
Abstract: In this talk I will present recent work examining how instructions, expectations, and associative learning jointly influence pain and aversive learning. In a series of experiments, we combined experimental manipulations with computational models to isolate the influences of these factors on subjective pain, aversive learning, and physiological responses. We found that these factors were supported by both interactions and dissociations in neural pathways. More recent work indicates that individual differences in state anxiety moderate these effects. I will discuss the clinical implications of these findings, as well as broader conclusions about how cognitive factors shape perception, including subjective outcomes such as pain.
[Video of the talk]

SCSB Lunch Series: Michael Strano, Ph.D.
2017-12-08 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, December 8, 2017
Time: 12:00pm – 1:00pm
Speaker: Michael Strano, Ph.D.
Affiliation: Carbon P. Dubbs Professor, Department of Chemical Engineering, MIT
Talk Title: Applications of Nanosensors to Understanding Biochemical Signaling Within the Human Body
Abstract: The human body is a vast network of biochemical signaling pathways dictating physiological and pathological processes. To probe this network, our research group has introduced Corona Phase Molecular Recognition, or CoPhMoRe, for discovering synthetic, heteropolymer corona phases that form molecular recognition sites at the nanoparticle interface. By screening libraries of synthetic heteropolymers chemically adsorbed onto single-walled carbon nanotubes (SWNT), we have engineered new optical biosensors that exhibit highly selective recognition for specific molecules, including riboflavin, L-thyroxine, dopamine, nitric oxide, sugar alcohols, estradiol, as well as proteins such as fibrinogen. The results have significant potential in that nanoparticles such as SWNT can be interfaced to biological systems at the sub-cellular level, allowing monitoring of sub-cellular, cellular, tissue, and whole-organism processes. With deep tissue penetration, we demonstrated our nanosensors in vitro with no photobleaching, and in vivo with no fluorescence degradation (400+ days).
Engineering the nanoparticle corona in this way offers significant potential to translate sensor technology to previously inaccessible environments. We have measured dopamine efflux from PC12 cells, which may allow monitoring of neuroendocrine production and signaling. Additionally, we have synthesized selective cortisol and progesterone sensors and are currently performing in vivo measurements of progesterone in mice. Cortisol has been implicated in numerous pathological conditions, including depression, post-traumatic stress disorder, bipolar disorder, and autism, whereas progesterone is the primary female sex hormone dictating fertility. Monitoring these, as well as other steroid hormones, could provide significant insight about the etiology of various endocrine-related pathologies. In the diabetes space, we have synthesized an insulin sensor and are currently designing glucose responsive insulins (GRI). Interfacing insulin sensors and a GRI with currently available continuous glucose monitors may revolutionize diabetes treatment, as insulin dosages will be more tightly controlled in a closed loop fashion. Last, I will discuss our current work in cancer. One major challenge in cancer is the ability to have an accurate and comprehensive picture of the intratumoral delivery and localization of chemotherapeutic drugs. The tumor heterogeneity has a significant impact on drug delivery, drug uptake, and therapeutic effectiveness. Our nanosensor platform can provide real-time spatiotemporal information about tumor metabolites and chemotherapeutic drug delivery. This feedback will give physicians and patients information about the tumor molecular response significantly earlier in a matter of hours or days compared to the weeks or months needed to see measurable size changes on CT or MRI.
