Simons Center for the Social Brain

SCSB Lunch Series: Nan Li, Ph.D.
2019-02-08 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 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 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: Danielle Tomasello, Ph.D.
2019-02-22 12:00 - 13:00 | 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 Leopold, Ph.D.
2019-02-27 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, February 27, 2019
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: David Leopold, Ph.D.
Affiliation: Senior Investigator, NIMH; Laboratory of Neuropsychology, NIMH
Host(s): Jitendra Sharma, Ph.D. and Rogier Landman, Ph.D.
Talk title: What’s in a Face Patch?
Abstract: Our laboratory has been investigating the electrophysiological activity of neural populations within fMRI-identified face patches in the monkey. The use of longitudinal microwire recordings permitted us to track the response profiles of single neurons over extended periods of time. As a consequence, we have been able to characterize the responses of individual cells to a wide range of visual stimuli and paradigms in multiple temporal cortex face patches. In my talk, I will focus on one finding that is shared among three spatially disparate face patches (AF, AM, ML), namely that the average face plays a central role in the basic tuning of neurons. I will demonstrate the temporal dynamics of this phenomenon over time scales ranging from milliseconds to months, speculate on a potential circuit mechanism, show its resistance to plasticity in the adult, and discuss its bearing on norm-based theories of human face recognition. Next, I will then show that the same neural populations, when faced with a different visual paradigm appear to undertake a very different type of feature analysis. I will make the case that theories of visual processing based on a narrow range of stimuli or testing paradigms are apt to be inherently fragile and contextual. Finally, I will briefly describe a method using fMRI in combination with single unit recording, which allows for a characterization of visually driven cell activity in a way that need not make reference to stimulus features.

SCSB Colloquium Series - Patricia K. Kuhl, Ph.D.
2019-03-13 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, March 13, 2019
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Patricia K. Kuhl, Ph.D.
Affiliation: Professor and Co-Director, Institute for Learning & Brain Sciences and Department of Speech and hearing Sciences, University of Washington, Seattle Washington.
Host: Dara Manoach, Ph.D.
Talk title: Early Language Acquisition and the Social Brain: An Inflection Point for the Brain’s Human Language Network.
Abstract: Human infants show a dramatic transition in early language development from an initial universal pattern of perception to one that is language-specific. During this time, human social interaction during exposure to language is critical to learning. Newly obtained resting state brain measures indicate that the propagation of electrical signals in the language network reverse direction at this exact same time in development. I’ll describe this inflection point in the brain’s developing language network and explore its impact and origins.
[Video of the talk]
Biography:
Dr. Patricia K. Kuhl holds the Bezos Family Foundation Endowed Chair in Early Childhood Learning, Co-Director of the UW Institute for Learning and Brain Sciences, and Professor of Speech and Hearing Sciences at the University of Washington in Seattle. She is internationally recognized for her research on early language learning and bilingual brain development, for pioneering brain measures on young children, and for studies that show how young children learn. She presented her work at two White House conferences (Clinton White House in 1997 and Bush White House in 2001). Dr. Kuhl is a member of the National Academy of Sciences, the American Academy of Arts and Sciences, the Rodin Academy, and the Norwegian Academy of Science and Letters. She is a Fellow of the American Association for the Advancement of Science, the Acoustical Society of America, the American Psychological Society, and the Cognitive Science Society. Dr. Kuhl was awarded the Silver Medal of the Acoustical Society of America in 1997. She received the University of Washington’s Faculty Lectureship Award in 1998. In 2005, she was awarded the Kenneth Craik Research Award from Cambridge University, and in 2007, the University of Minnesota’s Outstanding Achievement Award. In Paris in 2008, Dr. Kuhl was awarded the Gold Medal of the Acoustical Society of America for her work on early learning and brain development. In 2011, Dr. Kuhl received the IPSEN Foundation’s Jean-Louis Signoret Neuropsychology Prize, and in 2013 the William James Lifetime Achievement award. In 2014, Dr. Kuhl was awarded an Honorary Doctorate from Stockholm University, and in 2015 the George A. Miller Prize in Cognitive Neuroscience. Dr. Kuhl received the American Psychological Association’s Distinguished Scientific Contributions Award in 2018. Dr. Kuhl is co-author of The Scientist in the Crib: Minds, Brains, and How Children Learn (Harper Collins). Dr. Kuhl’s TED talk can be viewed at: http://www.ted.com/talks/patricia_kuhl_the_linguistic_genius_of_babies.html

SCSB Lunch Series: Nancy Padilla, Ph.D.
2019-03-22 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, March 22, 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: Nancy Padilla, Ph.D.
Affiliation: Simons Postdoctoral Fellow, Kay Tye Laboratory, Picower Institute of Learning and Memory, MIT.
Talk title: Investigating the neural circuits underlying social dominance in mice
Abstract: Most animals live in groups organized by social hierarchies. By acting according to their social rank, animals decrease unnecessary aggression and save energy. Although hierarchies are central to successful group dynamics, the neural basis of dominance behaviors remains unknown. Cross-species evidence suggests that the medial prefrontal cortex (mPFC) is crucial for social dominance behaviors. Given the role of the lateral hypothalamus (LH) in innate behaviors, and its connectivity with the mPFC, it is well positioned to modulate social behaviors in a rank-dependent manner. Using a reward competition assay, wireless electrophysiology and optogenetics in mice I am investigating the role of mPFC-LH pathway in social dominance. I will present data that suggest that the mPFC-LH drives winning during social competition.

SCSB Colloquium Series - Craig M. Powell, M.D., Ph.D.
2019-04-03 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, April 3, 2019
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Craig M. Powell, M.D., Ph.D.
Affiliation: Professor and Chair, Department of Neurobiology, University of Alabama at Birmingham School of Medicine
Hosts: Gloria Choi, Ph.D., Troy Littleton, Ph.D.
Talk title: Genetic Models of Autism: Molecules to Potential Therapeutics
Abstract: 16p11.2 copy number variants (CNV) are linked to neuropsychiatric disorders and are among the most prevalent CNVs in autism spectrum disorders (ASDs). Of many 16p11.2 genes, KCTD13 has been implicated as a major driver of neurodevelopmental phenotypes in zebrafish. The function of KCTD13 in mammalian brain, however, remains unknown. Here we delete Kctd13 in mice and demonstrate reduced synaptic transmission. Reduced synaptic transmission correlates with increased levels of RhoA, a KCTD13/CUL3 ubiquitin ligase substrate, and is reversed by RhoA inhibition, suggesting increased RhoA as an important mechanism. In contrast to a previous knockdown study, deletion of Kctd13 does not increase brain size or neurogenesis in mice or zebrafish. These findings implicate Kctd13 in regulation of neuronal function relevant to neuropsychiatric disorders and clarify the role of Kctd13 in neurogenesis and brain size. Our data also reveal a potential role for RhoA as a therapeutic target in disorders associated with KCTD13 deletion. Unpublished data will be presented on KCTD13 binding partner and ubiquitinating enzyme CUL3.
*** Please note that this talk will not be recorded

SCSB Lunch Series: Michael Halassa, M.D., Ph.D.
2019-04-12 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, April 12, 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: Michael Halassa, M.D., Ph.D.
Affiliation: Assistant Professor, Department of Brain and Cognitive Sciences, MIT.
Talk title: Frontothalamic interactions in cognitive control and flexibility
Abstract: Interactions between the cortex and thalamus are critical for sensation, action and cognition. However, most of our understanding of these interactions is in the context of sensory processing. My lab has focused on cortico-thalamic loops that are non-sensory, allowing us to discover new principles of thalamo-cortical interactions beyond sensory processing. In my talk, I will show how the thalamus plays previously unrecognized roles in implementing cognitive control and flexibility, which involve rapid reconfiguration of task-relevant prefrontal representations. I will give a few examples of this process, showing its generality across multiple species, and if time allows, discuss its relevance to disease processes.

SCSB Colloquium Series – Nouchine Hadjikhani, M.D., Ph.D.
2019-04-17 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, April 17, 2019
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Nouchine Hadjikhani, M.D., Ph.D.
Affiliation: Associate Professor of Radiology, Harvard Medical School

Host: Pawan Sinha, Ph.D.
Talk title: Look me in the eyes – or not?
Abstract: Abnormal eye contact is frequent in autism spectrum disorder. In this talk, I will present data supporting the hypothesis that an imbalance between the excitatory and the inhibitory systems (E/I) in infancy results in eye contact avoidance and abnormal development of the social brain, and present exciting preliminary studies showing how reestablishing the E/I balance may help the core symptoms of autism.
[Video of the talk]

Special Seminar: Clive R. Bramham, M.D., Ph.D.
2019-04-22 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Monday, April 22, 2019
Time: 4:00 pm-5:00 pm
Speaker: Clive R. Bramham, M.D., Ph.D.
Affiliation: Professor and Head of Neuroscience, Department of Biomedicine, University of Bergen, Norway
Host: Mriganka Sur, Ph.D., FRS
Talk title: Arc as a master regulator of neuronal plasticity: signaling protein or retroviral-like capsid.
Abstract: The immediate early gene, Arc, is a pivotal regulator of synaptic plasticity, memory, and cognitive flexibility. But what is Arc protein, how does it work? Recent work has provided surprising insights into the structural and biochemical properties of the Arc protein. Inside the neuron, Arc is protein interaction hub and dynamic regulator of synaptic plasticity. In radical contrast, Arc protein can also self-assemble into retrovirus-like capsids that are released in extracellular vesicles and capable of intercellular transfer of RNA. Resolving this dichotomy is of major importance for understanding how neuronal activity shapes connectivity in neural networks.
[Video of the talk]

SCSB Lunch Series: Anila D'Mello, Ph.D.
2019-05-10 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, May 10, 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: Anila D’Mello Ph.D.
Affiliation: Simons Fellow, John Gabrieli Laboratory, McGovern Institute for Brain Research, MIT.
Talk title: Characterizing Neural Adaptation in Autism Spectrum Disorder
Abstract: Sensory processing difficulties occur in about 90% of individuals with Autism Spectrum Disorder (ASD). Sensory hypersensitivities may negatively affect sleep, communication, and contribute to impairments in social interaction. Recent evidence suggests that sensory hypersensitivies in ASD may be associated with challenges in rapidly adapting to regularities in the environment. Here, I will discuss our work using functional magnetic resonance imaging (fMRI) to measure neural adaptation across social and non-social domains in adults with and without a diagnosis of autism. Our preliminary findings suggest that neural adaptation may be associated with autistic traits and symptom severity.

SCSB Colloquium Series - Guo-li Ming, Ph.D.
2019-05-15 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, May 15, 2019
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Guo-li Ming, Ph.D.
Affiliation: Perelman Professor of Neuroscience, University of Pennsylvania
Host: Hiruy Meharena, Ph.D.
Talk title: Modeling human brain development and brain disorders using 3D organoids.
Abstract: Human Induced pluripotent stem cells (hiPSCs) has the potential to generate all cell types of a human body under 2D culture conditions or form organ like structures- organoids, under 3D culture conditions. Brain organoid cultures from human iPSCs have been recently developed to recapitulate the cellular composition and the cytoarchitecture of the developing brain. These hiPSC based model systems offer unique advantages in understanding molecular and cellular mechanisms governing embryonic neural development and in modeling neurodevelopmental disorders, such as brain malformation and neuropsychiatric disorders. We have improved the organoid technology and developed a protocol to produce more mature forebrain-specific organoids. We have also developed tumor organoids from glioblastoma patients. I will discuss our recent work using these systems to understand human brain development and brain diseases.
*** Please note that this talk will not be recorded
Key words: brain organoids, brain development, Glioblastoma organoids, human iPSCs

SCSB Colloquium Series - Baljit Khakh Ph.D.
2019-05-29 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, May 29, 2019
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Baljit S. Khakh, Ph.D.
Affiliation: Professor of Physiology and Neurobiology, University of California, Los Angeles
Host: Mriganka Sur, Ph.D., FRS
Talk title: Astrocyte signaling within striatal microcircuits in vivo
Abstract: Hyperactivity and disturbances of attention are common behavioral disorders whose underlying cellular and neural circuit causes are not understood. We will report the discovery that striatal astrocytes drive such phenotypes through a hitherto unknown synaptic mechanism. We found that striatal medium spiny neurons (MSNs) triggered astrocyte signaling via GABAB receptors. Selective chemogenetic activation of this pathway in striatal astrocytes in vivo resulted in acute behavioral hyperactivity and disrupted attention. Such responses also resulted in up-regulation of the synaptogenic cue thrombospondin-1 (TSP1) in astrocytes, increased excitatory synapses, enhanced corticostriatal synaptic transmission, and increased MSN action potential firing in vivo. All of these changes were reversed by blocking TSP1 effects. Our data identify a form of bidirectional neuron-astrocyte communication, and demonstrate that acute reactivation of a single, latent astrocyte synaptogenic cue alters striatal circuits controlling behavior, revealing astrocytes and the TSP1 pathway as therapeutic targets in hyperactivity, attention deficit and related psychiatric disorders.

SCSB Lunch Series – Hector Penagos, Ph.D.
2019-09-06 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, September 6, 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: Hector Penagos, Ph.D.
Affiliation: Research Scientist, Wilson Laboratory, Picower Institute for Learning and Memory, MIT
Talk title: “Assessing thalamic participation in a joint hippocampus-retrosplenial cortex offline state ”
Abstract: The hippocampus and retrosplenial cortex have been implicated in a range of cognitive functions including navigation, planning and imagination. We recently discovered that the rodent hippocampus and retrosplenial cortex jointly transition into an offline state in response to increases in reward during spatial navigation tasks. At the neuronal ensemble level, this joint state is characterized by the reactivation of hippocampal spiking patterns linked to recent experiences. At the network level, both brain areas express oscillations previously thought to occur exclusively during sleep. This synchronous co-occurrence of sleep rhythms, along with the known role of the thalamus in sleep oscillations, raises the possibility that the thalamus might be involved in the generation of this waking state. In this talk, I will describe results that implicate the thalamic reticular nucleus in this hippocampal-retrosplenial offline state. These results extend the well-known role of the thalamus in coordinating activities across brain regions in sleep to the waking state.

SCSB Colloquium Series - Elizabeth Norton, Ph.D.
2019-09-11 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, September 11, 2019
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Elizabeth Norton, Ph.D.
Affiliation: Assistant Professor, Department of Communication Sciences and Disorders and Director of the Language, Education and Reading Neuroscience (LEARN) Lab, Northwestern University
Talk title: “Using naturalistic measures of brain and behavior to understand autism”
Abstract: Whereas diagnosis and therapy for autism spectrum disorder (ASD) occurs in live, interactive contexts between individuals, studies investigating the brain and behavioral basis of autism often occur in prescribed, solitary, experimental conditions. In this talk, I describe two lines of research, one neuroscience and one behavioral approach, that aim to examine ASD in more naturalistic conditions. The first line of research uses EEG to assess toddlers with and without ASD and their mothers while they interact naturally. During EEG, parents and children complete activities such as watching a movie or completing a puzzle together. Analyses compare child EEG power and parent-child EEG synchrony (phase locking) in frequency bands related to social interaction and attention. The second line of research examines language in the context of rapid automatized naming (RAN) tasks using eye-tracking. RAN requires automatic integration of a variety of language processes. These studies reveal that individuals with ASD and their family members, as well as women with the FMR1 premutation that carries risk for ASD, show altered patterns of eye movements during language processing despite similarities in verbal performance, to typically-developing individuals. Work using these less constrained methods could reveal new insights in to the features and etiology of ASD.

SCSB Colloquium Series - Alison Singer
2019-09-18 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, September 18, 2019
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Alison Singer
Affiliation: President, Autism Science Foundation
Talk title: “Autism From Generation to Generation”
Abstract: Ms. Singer will discuss how families’ experiences with autism have changed from the 1960’s to the present. While options and opportunities for people with autism are still severely lacking, there have been tremendous advances in awareness, diagnosis, treatment and services since autism was first identified. Alison will describe the different cultural climate her older brother faced when he was diagnosed in 1968 compared to her daughter’s experience being diagnosed in 2000. Over the past five decades individuals with autism have gained important rights and protections, but these improvements can quickly erode without continued family advocacy.
[Video of the talk]

Biography:
Alison Singer is Co-Founder and President of the Autism Science Foundation, a non-profit organization dedicated to funding innovative autism research and supporting the needs of people with autism. As the mother of a 22-year-old daughter with autism and legal guardian of her older brother with autism, she is a natural advocate. Singer served on the federal Interagency Autism Coordinating Committee (IACC) for 12 years, where she chaired the Safety and Housing Workgroups, and served on the subcommittee responsible for writing an annual strategic plan to guide federal spending for autism research. She currently serves on the executive boards of the Yale Child Study Center, the Seaver Autism Center at the Icahn School of Medicine at Mount Sinai, the Marcus Autism Center at Emory University, and the University of North Carolina Autism Research Center, as well as on the external advisory board of the CDC’s Center for Developmental Disabilities, and the New York State Immunization Advisory Committee. In addition, Singer serves on the board of directors of the International Society for Autism Research (INSAR) and chairs the INSAR Communications Committee. In 2012, the American Academy of Pediatrics named her an “autism champion.” In 2017 she received the INSAR “Outstanding Research Advocate” award and in 2018 she received the New York Families for Autistic Children Research Advocacy Award.
Prior to founding the Autism Science Foundation in 2009, she served as executive vice president of Autism Speaks and as a vice president at NBC. She graduated magna cum laude from Yale University with a B.A. in Economics and has an MBA from Harvard Business School. In 2018 she was elected to serve on the Board of Education of the Scarsdale Union Free Public School district. In her free time, she enjoys crossfit, kickboxing, and judging high school debate tournaments.

SCSB Lunch Series – Sasha Krol, Ph.D.
2019-09-27 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, September 27, 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: Sasha Krol, Ph.D.
Affiliation: Simons Fellow, Guoping Feng Laboratory, McGovern Institute for Brain Research, MIT.
Talk title: “Uncovering the origins of autism risk gene Ptchd1-associated aggression”
Abstract: Irritability or aggressive conduct affects 25-50% of children with autism spectrum disorder (ASD). Despite being highly disruptive, aggression in the context of ASD is poorly understood due to a lack of good models. Deletions in PTCHD1 contribute to ~1% of ASD cases with intellectual disability and can lead to hyper-aggression. I will present our work seeking to understand the origin of hyper-aggression in a mouse model of Ptchd1 deletion. We are testing whether dysfunction of hypothalamic circuitry, and in particular the VMHvl is responsible for Ptchd1-mediated, ASD-related aggression. We find that specifically inhibitory circuitry and not excitatory contributes to hyper-aggression. In addition we will present preliminary findings on the cellular function of Ptchd1.

SCSB Colloquium Series - Judith Burkart, Ph.D.
2019-10-02 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, October 2, 2019
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Judith Burkart, Ph.D.
Affiliation: University of Zurich, Department of Anthropology
Talk title: “Cooperative breeding and the evolution of human hypersociality – Insights from marmosets”
Abstract: Humans have evolved from a great ape-like ancestor 5-7 mio years ago. During this time, we not only evolved our uniquely human cognitive abilities, but also started to systematically share offspring care in the social group (i.e. engage in cooperative breeding). According to the cooperative breeding model of human evolution, this breeding system played a key role for the emergence of human hyper-sociality and cognition. I will present comparative data from nonhuman primates that support the cooperative breeding model, and show that across primates, shared offspring care is indeed associated with hyper-sociality, cooperation, and increased performance in socio-cognitive tasks. In the second part, I will zoom in on proximate, underlying mechanisms of hypersociality and cooperation in callitrichid monkeys (marmosets), who are the only other cooperatively breeding primates besides humans. The comparison of these proximate mechanisms in humans and cooperatively breeding primates are mandatory to fully understand the impact of cooperative breeding for human evolution, as well as for the use of marmosets as emerging neuroscientific model system.
[Video of the talk]
Bio: Judith M. Burkart is a Professor at the Department of Anthropology, University of Zurich. She studied Developmental Psychology in Fribourg, Switzerland, and got her PHD in Vienna, Austria. She is the head of the Evolutionary Cognition Group (https://www.aim.uzh.ch/de/research/ecg.html) and leader of the University’s Primate Station. The aim of her group is to contribute to a better understanding of the evolutionary origin of the human mind. To do so, they identify both similarities and differences in social, motivational and cognitive processes in human and nonhuman primates. One of our unique features, relative to the great apes, is cooperative breeding. A main focus therefore concerns the role of cooperative breeding, which we share with more distantly related primates. By studying the cooperatively breeding common marmosets and systematically comparing them with more independently breeding species, she aims at identifying processes that are systematically associated with shared infant care.

SCSB Colloquium Series - Sally Ozonoff, Ph.D.
2019-10-09 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, October 9, 2019
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Sally Ozonoff, Ph.D.
Affiliation: Endowed Professor of Psychiatry and Vice Chair for Research, University of California Davis
Talk title: “Advances in Early Detection of Autism Spectrum Disorder”
Abstract: Autism spectrum disorder (ASD) is typically diagnosed in the fourth year of life or later, but there is evidence from recent studies that symptoms are present much earlier, by the second year of life and earlier. There is now a strong thrust toward decreasing the age of diagnosis, with the hope that earlier detection will lead to earlier initiation of treatment and reduced disability. This presentation will cover new advances in detection of ASD in infants and toddlers, summarizing existing research and describing new results from an ongoing prospective study. Developmental challenges beyond ASD that occur in siblings will also be discussed. The talk with conclude with innovative approaches to early screening, including machine learning applications and automated detection of ASD-relevant behaviors in video.
[Video of the talk]

SCSB Lunch Series: Oliver Saunders Wilder, Ph.D.
2019-10-25 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, October 25, 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: Oliver Saunders Wilder, Ph.D.
Affiliation: Research Affiliate at the MIT Media Lab & Lead Technologist at Tools of the Mind.
Talk title: Using Interpersonal Physiology to Measure Socio-affective Dynamics: Techniques, Findings, and Opportunities
Abstract: Individuals with Autism Spectrum Disorder (ASD) often have great difficulty interpreting and using nonverbal communication, understanding and navigating social relationships, and making sense of their own and others’ emotions. Many of these challenges can be understood in terms of difficulty with social reciprocity, the ability to attend to, predict, and respond appropriately to the mental states of others, and are present in both more severely affected as well as “higher-functioning” individuals with ASD who have little or no cognitive impairment. A key challenge to studying the development of social reciprocity is that social interactions are fundamentally transactional, taking place within a system rather than in isolation, and that people affect and are affected by their interactions with others. A growing body of work in interpersonal physiology – the study of psychophysiological signals across two or more people – can offer a powerful new means for non-invasive ambulatory assessment of socio-affective processes in a variety of laboratory and naturalistic settings. I will present a novel statistical modeling technique for quantifying interpersonal physiology, and discuss several applications of this technique, including a study of young children with and without an autism diagnosis and their parent, a pilot study of pre-term infants and caregivers in a neonatal intensive care unit, and a clinical application our new real-time physiological synchrony system for interpersonal biofeedback in mental health counseling.
Click here for CV.

SCSB Lunch Series: Dara S. Manoach, Ph.D.
2019-11-08 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, November 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: Dara S. Manoach, Ph.D.
Affiliation: Professor of Psychology, Department of Psychiatry at Harvard Medical School.
Talk title: Targeting sleep oscillations to improve cognition in neurodevelopmental disorders.
Abstract: Sleep oscillations are novel pathophysiological targets for therapy to improve cognition. This talk will summarize our understanding of how sleep oscillations interact to consolidate memory and illustrate this with findings from our recent clinical trial in schizophrenia and ongoing studies of autism spectrum disorder. Finally, I will present pilot data from a study of auditory stimulation during sleep to improve memory. Our findings demonstrate that effective therapies will need to enhance sleep oscillatory dynamics and restore function at the network level.

SCSB Colloquium Series - Devanand Manoli, M.D., Ph.D.
2019-11-13 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, November 13, 2019
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Devanand Manoli, M.D., Ph.D.
Affiliation: Assistant Professor, Department of Psychiatry and Weill Institute for Neuroscience, Center for Integrative Neuroscience, Kavli Institute for Fundamental Neuroscience, University of California, San Francisco
Hosts: Steven Flavell, Ph.D., Mriganka Sur, Ph.D., FRS
Talk title: Understanding the neural basis of social attachment.
Abstract: Social attachments play a central role in most, if not all, levels of human interaction, from parent-child attachment, friendship and social affiliation, to enduring partnerships with mates. Devastating conditions such as autism spectrum disorders (ASD) and schizophrenia often manifest with a collapse of inter-personal interactions. It has been difficult to study social attachment because traditional genetic lab model animals do not exhibit adult social attachment behaviors. Thus, the analysis of social attachment has been resistant to genetic and neurobiological approaches. Prairie voles, in contrast, display social attachment as adults, such that mating partners form an enduring pair bond and display complex attachment behaviors, such as social monogamy, bi-parental care, and stress responses when social bonds are disrupted. In humans and many species, the peptide hormones oxytocin and vasopressin facilitate social behaviors, and in prairie voles, also facilitate the formation of pair bonds between mates. We use targeted molecular genetics in voles to generate prairie voles with mutations in genes associated with pair bonding, as well as with psychiatric disorders such as ASD to understand how these genes function in the circuits mediating social attachment behaviors.
[Video of the talk]

SCSB Lunch Series: Ann Graybiel, Ph.D.
2019-11-22 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, November 22, 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: Ann Graybiel, Ph.D.
Affiliation: Institute Professor, MIT; Investigator, McGovern Institute for Brain Research.
Talk title: The Striatum and the Motivation to Act.
Abstract: The striatum was once thought to be a primitive part of the forebrain, despite evidence that basal ganglia dysfunction underlies major extrapyramidal disorders. Our work has contributed to the surprising realization that the striatum actually has a sophisticated compartmental structure, that striatal circuits are implicated in decision-making and in neuropsychiatric as well as motor disorders, and that special modules in the striatum, called striosomes, are focal points in circuits linking mood-related neocortex with midbrain dopamine-containing neurons and other neuromodulatory regions. The striatum thus modulates a broad range of circuits affecting our behavioral state in health and disease.

SCSB Colloquium Series - Neville Sanjana, Ph.D.
2019-12-04 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, December 4, 2019
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Neville Sanjana, Ph.D.
Host: Feng Zhang, Ph.D.
Affiliation: Core Faculty Member, New York Genome Center; Assistant Professor of Biology, Neuroscience and Physiology, New York University
Talk title: Chromatin modifiers in autism and combining pooled CRISPR screens with single-cell chromatin accessibility profiling
Abstract: One of the most commonly mutated genes in autism is the chromatin remodeler CHD8. Despite the prevalence of CHD8 mutations, we have little insight into how CHD8 loss impacts genome organization and the functional consequences of these molecular alterations in neurons. Here, we combine gene editing in human pluripotent stem cells and rapid cortical neuron differentiation to create an isogenic model of CHD8 loss in neurons. By measuring changes in chromatin accessibility and gene expression, we identified hundreds of genes with altered expression, including many involved in neural development and excitatory synaptic transmission. Using field recordings and single-cell electrophysiology, we found a 3-fold decrease in firing rates and synaptic activity in CHD8+/– neurons. We also observed a similar firing rate deficit in primary cortical neurons from CHD8+/– mice. These alterations in neuron and synapse function after CHD8 hemizygous loss can be rescued by CHD8 overexpression.
Given CHD8’s role in chromatin remodeling, we used the assay of transposable and accessible chromatin sequencing (ATAC-seq) to map changes in open chromatin genome-wide. In differentiated human neurons, we found that CHD8 hemizygous loss results in a large increase in open chromatin across the genome with the greatest change in compaction near the gene Autism Susceptibility Candidate 2 (AUTS2), a transcriptional regulator that has previously been implicated in autism.
In the last part of my talk, I’ll address the challenge of scaling up this approach: CHD8 is just one gene and many different chromatin remodeling and modifying enzymes have been implicated in autism. To address this, we recently developed a scalable, cost-effective method called CRISPR-sciATAC that links genome-wide chromatin accessibility to genetic perturbations through simultaneous capture and barcoding of ATAC-seq fragments and CRISPR guide RNAs. Using a species-mixing experiment, we show that CRISPR-sciATAC results in a low doublet rate. Finally, we use CRISPR-sciATAC to knock-out 21 different chromatin modifiers and generate chromatin accessibility data from ~12,000 single cells.
Publications: http://sanjanalab.org/papers.html

SCSB Lunch Series: Jitendra Sharma, Ph.D.
2019-12-06 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, December 6, 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: Jitendra Sharma, Ph.D.
Affiliation: Research Scientist, Mriganka Sur Laboratory, Picower Institute for Learning and Memory, MIT.
Talk title: “Investigating circuits related to autism in primate models”
Abstract: The incidence and societal impact of autism and other neurodevelopmental disorders continue to increase despite years of research. Modeling these primarily human brain disorders in animals will require investigation with diverse species. Primates exhibit a sophisticated social behavior repertoire and closer brain homology to humans, and can, therefore, function as crucial bridge species to determine neurobiological mechanisms underlying neurodevelopmental disorders; develop and test novel therapeutic approaches; and ultimately, translate basic research into safe and effective treatments. I will present our recent successes in developing and characterizing a transgenic model of a syndromic form of autism in old-world primates. Besides exhibiting shades of behaviors that broadly parallel autism, this model reinforces the conclusion that genetic deficits lead to atypical brain circuits and their functional connectivity. Based on these and other findings, in the second part of my presentation, I will describe our early effort in adapting and creating new tools for the experimental manipulation of brain circuits related to autism that span diverse aspects of sensory, cognitive and social processing, in marmosets.

SCSB Colloquium Series - Charles Nelson, Ph.D.
2020-02-12 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, February 12, 2020
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Charles Nelson, Ph.D.
Affiliation: Professor of Pediatrics, Boston Children’s Hospital; Director of Research, Developmental Medicine Center
Talk title: “Sensitive periods in human development: A case study of early psychosocial deprivation”
Abstract: Experience is the engine that drives much of postnatal brain development. When children are deprived of key (i.e., experience-expected) experiences, particularly during critical periods of development, brain and behavioral development can be derailed. There is perhaps no more egregious form of deprivation than being raised in large, state-run institutions.
In my talk, I will introduce a project launched nearly 20 years ago, based in Bucharest, Romania. In the Bucharest Early Intervention Project three groups of Romanian children are being studied: infants abandoned to institutions and who remain in institutional care; infants abandoned to institutions but then placed in high quality foster care; and infants who have never been institutionalized. These three groups have been studied through age 16, with a 20 year follow up being planned. In my talk I will introduce the overall project, including its conceptual framework, its experimental design, the ethics involved in conducting this work and the nature of the intervention we deployed. I will then briefly summarize findings from several key domains, including brain development, cognitive development, social-emotional development, psychopathology, and stress physiology.
[Video of the talk]

SCSB Lunch Series: Jesse Snedeker, Ph.D.
2020-02-21 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, February 21, 2020
Time: 12:00pm – 1:00pm
Location: Simons Center Conference Room, Building 46, Room 6011, 6th Floor, MIT (43 Vassar Street, Cambridge, 02139 MA)
Speaker: Jesse Snedeker, Ph.D.
Affiliation: Professor, Department of Psychology, Harvard University
Talk title: “Moment-to-moment language comprehension in highly verbal children with autism: Studies of prosody, pragmatics and the role of context”
Abstract: In developmental psychology and psycholinguistics, autism is often invoked as evidence that the core structural aspects of human language (phonology, syntax and word meaning) can be disassociated from more peripheral or social aspects of language use (often linked to pragmatics, prosody or the use of context). These arguments begin by noting that a substantial minority of children with autism have strong structural language skills but, by definition, have impairments in social communication. For the past ten years I have been exploring this hypothesis by testing highly-verbal children with autism, using the visual world paradigm, and focusing on simple aspects of spoken language comprehension that involve prosody, pragmatic inferences or contextual knowledge. I’ll discuss how these results constrain our understanding of language and autism and introduce our ongoing work on EEG indices of linguistic prediction.

SCSB Colloquium Series - Kevin Bender, Ph.D.
2020-02-26 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Wednesday, February 26, 2020
Time: 4:00 pm-5:00 pm, followed by reception
Speaker: Kevin Bender, Ph.D.
Affiliation: Associate Professor of Neurology, University of California, San Francisco
Hosts: Elly Nedivi, Ph.D.
Talk title: Sodium channel dysfunction in neurodevelopmental disorders
Abstract: De novo mutations in the gene SCN2A are associated with a range of neurodevelopmental disorders, including epilepsy, autism spectrum disorder (ASD) and intellectual disability. Interestingly, these different disorders are often associated with different effects on SCN2A function, with gain of function variants most commonly associated with epilepsy and loss of function variants most commonly associated with ASD and intellectual disability. Our lab has been interested primarily in understanding how loss of function variation in SCN2A affects the nervous system and understanding whether therapeutics can be developed to treat such disorders.
[Video of the talk]

Canceled: SCSB Colloquium Series – Joshua Hartshorne, Ph.D.
2020-03-11 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Please note that this event is canceled and will be rescheduled for a later date
Speaker: Joshua Hartshorne, Ph.D.
Affiliation: Assistant Professor, Department of Psychology & Neuroscience, Boston College
Host: Ev Fedorenko, Ph.D.
Talk title: Critical periods in language, cognitive development, and massive online experiments
Abstract: Only a few years ago, it was widely accepted that cognitive abilities develop during childhood and adolescence, with cognitive decline beginning at around 20 years old for fluid intelligence and in the 40s for crystalized intelligence. The obvious outlier was language learning, which appeared to begin its decline in early childhood. All these claims have been challenged by a recent flurry of studies — both from my lab and others. In particular, the ability to collect large-scale datasets has brought into sharp relief patterns in the data that were previously indiscernible. The fluid/crystalized intelligence distinction has broken down: at almost any age between 20 and 60, some abilities are still developing, some are at their peak, and some are in decline (Hartshorne & Germine, 2015). Most surprisingly, evidence suggests that the ability to learn syntax is preserved until around 18 (Hartshorne, Tenenbaum, & Pinker, 2018). This has upended our understanding of language learning and its relationship to the rest of cognitive development. In this talk, I review recent published findings, present some more recent unpublished findings, and try to point a path forwards. I also discuss the prospects for massive online experiments not just for understanding cognitive development, but for understanding cognition in general.

To be rescheduled: SCSB Lunch Series: Jakob Voigts, Ph.D.
2020-03-20 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: To be rescheduled
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: Postdoctoral Fellow, McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, MIT
Talk title: Conjunctive processing of spatial and goal-directed task variables in mouse retrosplenial cortex
Abstract: Retrosplenial cortex is the main hub by which sensory and motor information is related to the allocentric representations of the world. Neurons in RSC have been shown to encode mixtures of egocentric and world-centric variables, suggesting that RSC learns to represent specific features of the animal’s environment in order to guide an animal’s navigation choices. Here, by using a multi-modal spatial task we show that single neurons in RSC encode generalized spatial, sensory, motor, as well as task-specific features.
