Simons Center for the Social Brain

SCSB Lunch Series: Dr. Jen Yong
2026-02-13 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 13, 2026
Time: 12:00pm – 1:00pm
Location: Simons Center Conference room 46-6011 + Zoom [https://mit.zoom.us/j/98419153925]
Speaker: Jen Yong, Ph.D.
Affiliation: Simons Postdoctoral Fellow, Huh Lab, Harvard Medical School
Talk title and abstract to be provided later…

SCSB Colloquium Series: Vikaas Sohal, M.D., Ph.D.
2025-12-10 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Wednesday, December 10, 2025
Location: 46-3002 (Singleton Auditorium)
Speaker: Vikaas Sohal, M.D., Ph.D.
Affiliation: Professor, Department of Psychiatry, Weill Institute for Neurosciences, University of California San Francisco
Host: Dr. Linlin Fan
Talk title and abstract to be provided later….

SCSB Lunch Series with Dr. Haoran Xu and Dr. Beizhen Zhang - Investigating Neural Circuit Abnormalities in SHANK3 Mutant Marmosets
2025-12-05 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, December 5, 2025
Time: 12:00pm – 1:00pm
Location: Simons Center Conference room 46-6011 + Zoom [https://mit.zoom.us/j/95992863075]
Speakers: Haoran Xu, Ph.D., Research Scientist & Beizhen Zhang, Ph.D., Postdoctoral Fellow
Affiliation: Desimone Lab, McGovern Institute, MIT
Talk title: Investigating Neural Circuit Abnormalities in SHANK3 Mutant Marmosets
Abstract: Phelan-McDermid Syndrome (PMS) is a neurodevelopmental disorder caused by mutations or deletions in the SHANK3 gene, a key component for maintaining synaptic structure and neural circuit integrity. Individuals with PMS exhibit profound social communication deficits, intellectual disability, and sensory abnormalities, yet the neural circuit mechanisms underlying these symptoms remain elusive. In this talk, I will present our ongoing work using SHANK3 mutant marmosets as a primate model to probe these circuit dysfunctions. We implanted four 64-channel ECoG arrays across temporal and prefrontal regions in mutant and wild-type animals and examined their neural dynamics during social perception, cognitive, and auditory tasks. Despite showing normal gaze patterns while viewing faces or movies, SHANK3 mutants exhibited reduced high-gamma activity in face-selective regions and weakened social representations in both the prefrontal (PFC) and inferotemporal (IT) cortices. During working memory tasks, mutants performed more poorly, with their deficits linked to elevated alpha and high-gamma power in the PFC during the delay period. In the auditory domain, they showed hypoactivity in auditory cortical areas but paradoxical hyper-responsivity to noise-like sounds in the PFC and visual regions, suggesting impaired inhibition. Together, these findings reveal how SHANK3 disruption alters distributed neural circuits underlying social, cognitive, and sensory processing, offering a window into the circuit-level basis of PMS and related neurodevelopmental disorders.

SCSB Lunch Series with Dr. Marvin Lavechin: Small babies, big data: decoding early vocalizations with speech technology
2025-11-14 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, November 14, 2025
Time: 12:00pm – 1:00pm
Location: Simons Center Conference room 46-6011 + Zoom [https://mit.zoom.us/j/98894785862]
Speaker: Marvin Lavechin, Ph.D.
Affiliation: Simons Postdoctoral Fellow, Computational Psycholinguistics Lab, Department of Brain and Cognitive Sciences, MIT
Talk title: Small babies, big data: decoding early vocalizations with speech technology
Abstract: Babbling is a critical milestone during which infants explore moving their articulators to produce increasingly complex sounds before producing their first words around 12 months. As of today, studying vocal development requires the costly and labor-intensive process of manually transcribing children’s linguistic productions, which often limits research to small sample sizes. In this talk, I’ll present my ongoing efforts to build a fully automated speech processing pipeline to enable large-scale studies of vocal development from naturalistic day-long recordings. The talk follows three stages of inquiry. First, detecting when children vocalize – a prerequisite for studying what they say (past work). Second, characterizing the sounds they produce (current work). Third, measuring when language-specificity emerges in their vocalizations (future work). With this pipeline, I hope to address two long-standing questions: To what extent do individuals follow shared trajectories in phonological development? And when do infants start exhibiting distinct babbling patterns across different languages? Beyond theoretical implications, these insights will also allow investigation of early vocal markers associated with atypical language development.

SCSB Colloquium with Dr. Erin Hecht: Domestic dogs as a window on nature and nurture in mammalian brain evolution
2025-11-12 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Researcher Erin Hecht has a new paper in HEB about different breeds of dogs having different brain organization. She is pictured in her office with miniature Australian Shepherds Lefty and Izzy..Jon Chase/Harvard Staff Photographer.
Date: Wednesday, November 12, 2025
Location: 46-3002 (Singleton Auditorium)
Speaker: Erin Hecht, Ph.D.
Affiliation: Assistant Professor, Department of Human Evolutionary Biology, Harvard University
Host: Dr. Ev Fedorenko
Talk title: Domestic dogs as a window on nature and nurture in mammalian brain evolution
Abstract: Disentangling the relative contributions of heritable and environmental factors has been a central challenge in biology and neuroscience, especially for large-brained, behaviorally complex species. Domestic dogs offer a special window on this question, since distinct lineages have been artificially selected for different, specific skills which have an innate basis but are nonetheless dependent on environmental exposure and training. This talk will cover our lab’s recent brain-behavior findings in dogs. We will discuss neural traits resulting from selection for working skills, the separate and interacting effects of training and selection, neural correlates of trainability, service work, and communication, and a white matter pathway in the canine brain which appears to be analogous to the human arcuate fasciculus. We will also draw some comparisons with our lab’s ape neuroscience research and consider implications for human brain evolution.

SCSB Colloquium Series with Dr. Aakanksha Singhvi: Glial molecular heterogeneity and roles in neural function, aging, and Parkinson’s disease
2025-10-29 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Wednesday, October 29, 2025
Location: 46-3002 (Singleton Auditorium)
Speaker: Aakanksha Singhvi, Ph.D.
Affiliation: Associate Professor, Basic Sciences Division, Fred Hutch Cancer Research Center
Host: Dr. Steve Flavell
Talk title: Glial molecular heterogeneity and roles in neural function, aging, and Parkinson’s disease
Abstract: Molecular interactions between the two major cell types of the nervous system, glia and neurons, underlie neural development and functions. Compared to neurons, however, molecular understanding of glial functions remains sparse. Beyond fundamental insight into how the nervous system works, this critical knowledge gap is also disease-relevant, given that glial dysfunction is seen in many neurological disorders.
My lab investigates glia biology in vivo at single-cell resolution using C. elegans as a powerful molecular-genetic platform that we helped establish. We previously identified glial factors that modulate neuron properties, uncovered that tricellular epithelia-glia-neuron mechanobiology coupling impacts neural aging, and built the complete molecular atlas of C. elegans glia – which revealed extensive molecular heterogeneity and sex-dimorphism across nervous system glia.
We had also previously discovered that glial engulfment/pruning is a conserved function in C. elegans and found that glia dynamically modulate engulfment based on neuron activity. Engulfment of neuron-fragments is a critical and disease-linked, but molecularly less-defined, glial function. We now report our finding that multiple genes linked to Parkinson’s disease (PD), the fastest growing neurodegenerative disorder, act in glia to regulate glial engulfment downstream of neuron activity. Further, mechanistically these genes act differently in glia compared to their reported neuronal roles, via a pathway conserved in humans. Thus, our findings link glial engulfment to PD; and highlight the importance of evaluating disease-gene functions by (glial) cell-context for complete assessment of their roles in disease etiology.

SCSB Lunch Series with Dr. Caroline Robertson: Semantic Drivers of Gaze in Natural Environments
2025-10-17 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, October 17, 2025
Time: 12:00pm – 1:00pm
Location: Simons Center Conference room 46-6011 + Zoom [https://mit.zoom.us/j/93701332166]
Speaker: Caroline Robertson, Ph.D.
Affiliation: Associate Professor of Psychological and Brain Sciences, Dartmouth College
Talk title: Semantic Drivers of Gaze in Natural Environments
Abstract: Is gaze a window into the cognitive landscape of a viewer? While it is well established that visual features of the external environment guide attention, the extent to which gaze reflects our endogenous cognitive priorities remains less clear. Naturalistic contexts are ideal for studying these endogenous factors, as individuals must draw on their own conceptual knowledge bases and priorities during active visual selection. In this talk, I will present two ongoing eye-tracking studies that leverage computational language models to uncover the cognitive priorities guiding gaze in individuals with and without autism in naturalistic contexts. First, in immersive, real-world environments, eye-tracking reveals idiosyncratic, trait-like “gaze fingerprints” in individuals with and without autism, which are partly explained by the conceptual feature space of a large language model, capturing unique variance beyond spatial and vision-based models. Second, in dyadic conversations, mobile eye-tracking shows that gaze to the conversation partner’s face is modulated by the ongoing semantic context of the exchange, including linguistic surprisal – with differences between individuals with and without autism. Together, these findings position gaze as a window into the semantic and predictive processes that shape attention, providing new leverage for modeling individual differences in natural contexts.

SCSB Colloquium Series with Dr. Carla J. Shatz: Surprise at the Synapse: classically immune genes in neurons and synapse pruning
2025-10-08 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Wednesday, October 8, 2025
Location: 46-3002 (Singleton Auditorium)
Speaker: Carla J. Shatz, Ph.D.
Affiliation: Professor of Biology and Neurobiology, Stanford University
Host: Dr. Mriganka Sur
Talk title: Surprise at the Synapse: classically immune genes in neurons and synapse pruning
Abstract:
Carla J. Shatz and her lab, Bio-X, Departments of Biology and Neurobiology, Stanford University
During brain development, circuits form sequentially, first by creating a basic scaffold of connectivity according to strict molecular axon guidance cues. Subsequently final details of each circuit emerge by pruning and sculpting synapses. This synapse selection process is also genetically specified but in contrast to axon guidance, the program requires neural activity. Prenatally even before vision the brain generates its own internal neural activity patterns- in the form of spontaneous retinal waves- to jump-start the sculpting process. Postnatally, visual experience takes over to sharpen brain wiring during critical periods. Neural activity and sensory experience regulate expression of sets of genes including several previously thought to act only in the immune system. These genes- including Major Histocompatibility Class I family members and the MHCI receptor Paired immunoglobulin-like receptor B- are required in neurons for pruning and sculpting synapses during development. In human cerebral cortex, MHCI proteins (= HLA class I) and LilrB2 (a PirB homolog) are expressed at excitatory synapses where, by analogy, they may also collaborate in synapse pruning. Neurons in human cortical organoids express these molecules and in an in vitro model of maternal immune activation, exposure to inflammatory cytokines results in a striking increase in neuronal expression of HLAI family members, as well as in altered patterns of spontaneous neural activity. It is possible that changes in expression and/or function of these molecules in the brain lead to alterations in synapse pruning that could underlie developmental disorders. In SFARI Gene, LilrB2 and several HLA class I genes are categorized as “strong” ASD candidates, with statements that these genes contribute solely to immune system dysfunction. In view of the observations above, a neuronal function for these genes merits further study. Supported by NIH EY02858, NIA AG065206, Mathers Charitable Foundation, Sapp Family Foundation, Phil and Penny Knight Stanford Initiative for Brain Resilience.
Bio: Carla J. Shatz is Sapp Family Provostial Professor of Biology and Neurobiology and the Director Emerita of Bio-X, Stanford University’s pioneering interdisciplinary biosciences program. She received her B.A. in Chemistry from Harvard University (Radcliffe College) in 1969 and then an M.Phil. (Physiology; 1971) from University College London on a Marshall Scholarship. In 1976 she received her Ph.D. in Neurobiology from Harvard Medical School, mentored by David Hubel and Torsten Wiesel. Shatz joined the faculty at Stanford in 1978, then moved to University of California Berkeley in 1992, and to Harvard Medical School in 2000 as the first woman to Chair the Department of Neurobiology. She returned to Stanford in 2007 to direct Bio-X. Dr. Shatz is a neuroscientist who has devoted her career to understanding the dynamic interplay between genes and environment that shapes brain circuits – the very essence of our being. Shatz has earned many honors and awards, including election to the National Academy of Sciences, the American Philosophical Society and the Royal Society of London. She received the Gruber Neuroscience Prize in 2015. In 2016, she was the recipient of the Champalimaud Vision Prize, as well as the Kavli Prize in Neuroscience for the discovery of mechanisms that allow experience and neural activity to remodel brain circuits. In 2018, she received the Harvey Prize in Science and Technology from the Technion Israel Institute of Technology.

Special Talk with Dr. Anne Desmazieres: Neuronal activity and immune cues modulate neuron-microglia communication at the node of Ranvier, shaping its role in repair
2025-09-24 14:00 - 15:00 | Picower Seminar Room, 46-3310, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Wednesday, September 24, 2025
Location: 46-3310
Time: 2:00pm-3:00pm EDT
*This Special talk is co-hosted by the Picower Institute for Learning and Memory and the Simons Center for the Social Brain
Speaker: Anne Desmazieres., Ph.D.
Affiliation: Paris Brain Institute/Institut du Cerveau (ICM), Team Regain in MS
Talk title: Neuronal activity and immune cues modulate neuron-microglia communication at the node of Ranvier, shaping its role in repair
Abstract: Multiple Sclerosis (MS) is an inflammatory, demyelinating and neurodegenerative disease of the central nervous system (CNS). While an endogenous repair process exists following demyelination in MS, it is incomplete and varies between individuals. Understanding the mechanisms of remyelination and neuroprotection is therefore crucial to promote repair in patients.
In MS, the nodes of Ranvier, which support the fast axonal conduction, are disrupted but can reorganize early during repair, even before remyelination proceeds. Furthermore, microglia, the central nervous system resident immune cells, are key players in the disease, as they can engage in pro-inflammatory as well as pro-regenerative processes.
Our recent work identified nodal structures as a preferential site for microglia-neuron interaction in both mouse and human. We now demonstrate that neuronal activity promotes microglia-node interaction and the switch towards pro-regenerative microglia. Conversely, adaptive immune cues impair microglia-node interaction in an inflammatory MS model and the extent of these interactions at the onset of remission correlates with recovery. Taken together, our findings identify factors that influence microglia-neuron crosstalk in disease and suggest that neuronal activity supports remyelination not only by directly regulating oligodendroglia, but also by modulating microglial behavior during repair.

SCSB Lunch Series with Dr. Gabriel Stine: Cerebellar adjustment of neocortical dynamics during non-motor learning
2025-09-19 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, September 19, 2025
Time: 12:00pm – 1:00pm
Location: Simons Center Conference room 46-6011 + Zoom [https://mit.zoom.us/j/95726791202]
Speaker: Gabriel Stine, Ph.D.
Affiliation: Simons Postdoctoral Fellow, Jazayeri Lab, McGovern Institute, MIT
Talk title: Cerebellar adjustment of neocortical dynamics during non-motor learning
Abstract: The enlargement of the lateral cerebellum and its extensive connections with the majority of neocortex is one of the most salient features of the primate brain. Yet, we know almost nothing about how the cerebellum influences neocortical activity to support cognitive function. In motor control, the cerebellum is known to form internal models that enable us to quickly correct errors in ongoing movements and gradually adapt to new environments. We hypothesize that the cerebellum serves a similar function for cognition by forming internal models that error-correct and adapt neocortical dynamics that underlie non-motor processes. In this talk, I’ll present our ongoing efforts to test this hypothesis using large-scale, simultaneous neuropixels recordings throughout the cerebello-thalamocortical pathway as monkeys perform a novel timing adaptation task. Our preliminary findings suggest that the dentate nucleus (DN)—the primary output of the cerebellum to the neocortex—conveys signed temporal prediction errors in response to predictable events in the environment. This error signal predicts changes in the speed of ramping activity in the parietal cortex and error-corrections in the animal’s timing behavior. Finally, electrical microstimulation of DN improved timing behavior, mimicking error correction. The results offer a first glimpse into how the cerebellum uses internal models to control neocortical dynamics related to non-motor processes.

SCSB Colloquium Series with Dr. Carol Wilkinson: Early EEG markers of autism from lab to primary care
2025-09-10 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Wednesday, September 10, 2025
Location: 46-3002 (Singleton Auditorium)
Speaker: Carol Wilkinson, M.D., Ph.D.
Affiliation: Assistant Professor in Pediatrics and Attending in Developmental Medicine, Boston Children’s Hospital
Talk title: Early EEG markers of autism from lab to primary care
Abstract: How can EEG be used to inform early brain development and facilitate early identification of neurodevelopmental disorders, including autism? In this talk, I will present recent published and unpublished work using EEG during the first three year of life to both characterize early brain development and explore its potential for identifying developmental delay or autism early on. I will briefly discuss overlap in findings from typical development with genetic disorders including Fragile X Syndrome and Down Syndrome. Finally, I will present unpublished data from our Baby Steps study, which collects longitudinal EEG data in the primary care clinic setting in order to assess the feasibility and effectiveness of using EEG as a screening tool in the clinical setting.

SCSB Lunch Series with Dr. Gwangsu Kim: Neural substrate of visual valence in the primate amygdala
2025-09-05 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, September 5, 2025
Time: 12:00pm – 1:00pm
Location: Simons Center Conference room 46-6011 + Zoom [https://mit.zoom.us/j/92816748974]
Speaker: Gwangsu Kim, Ph.D.
Affiliation: Simons Postdoctoral Fellow, DiCarlo Lab, McGovern Institute, MIT
Talk title: Neural substrate of visual valence in the primate amygdala
Abstract: The primate amygdala is known to encode the valence of sensory stimuli, particularly through conditioning-based associative learning. However, the neural mechanism by which valence is assigned to unconditioned visual inputs—lacking explicit value association—remains unclear. Here, we report that primate amygdala neurons systematically assign valence to unconditioned naturalistic visual inputs without explicit value conditioning. Electrophysiological recordings from the primate amygdala and inferior temporal cortex (IT) during the presentation of 400 novel images revealed that some amygdala neurons exhibit reliable visual tuning comparable to IT neurons. The amygdala responses were predictable using task-optimized models of IT, supporting its role as a subsequent layer in the visual processing hierarchy. Notably, significant subpopulations of visual amygdala neurons jointly encoded valence, with their cross-modal valence tuning linearly predictable from their visual tuning profiles. These findings suggest that the amygdala systematically process valence of unconditioned visual stimuli, alongside its role in associative learning.
Bio: Gwangsu received his BSc (2017) and PhD (2023) in Physics from Korea Advanced Institute of Science and Technology. He joined the MIT McGovern institute in 2024 as a postdoctoral researcher. During his PhD, he studied brain-like functional representations of sensory stimuli in deep neural networks and their underlying computational principles.

SCSB Colloquium Series with Dr. Shawn Liu: Decoding the Epigenome in Brain Function and Disorders
2025-05-21 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Wednesday, May 21, 2025
Location: 46-3002 (Singleton Auditorium)
Speaker: X. Shawn Liu, PhD
Affiliation: Joan and Paul Marks, MD ’49 Assistant Professor, Columbia University, Department of Physiology and Cellular Biophysics
Host: Dr. Rudolf Jaenisch
Talk title: Decoding the Epigenome in Brain Function and Disorders
Abstract: Epigenetics is a fundamental mechanism enabling our genome to integrate nature and nurture. It plays a critical role during brain development and perturbations of this mechanism can result in numerous brain disorders. Our laboratory aims to decode the epigenome to understand how genetic information is read in normal physiology and manipulated in diseases. We have developed a series of epigenome editing tools to help dissect the functional significance of epigenetic events. We are combining these molecular tools with genetic and genomic approaches to explore epigenetic mechanisms underlying normal brain functions, and to uncover the epigenetic basis of diseases to accelerate the development of therapeutics. We mainly use human ESC- or iPSC-based system and genetically engineered mouse models to tackle these questions. One of our recent projects revealed the function of DNA methylation in fear memory engram in the basolateral amygdala. Another project demonstrated a methylation editing-based strategy for the treatment of ALS/FTD caused by GGGGCC repeat expansion.

SCSB Lunch Series with Dr. Christopher Fell: Repurposing natural enzymes for large genomic edits
2025-05-16 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, May 16, 2025
Time: 12:00pm – 1:00pm
Location: Simons Center Conference room 46-6011 + Zoom (https://mit.zoom.us/j/91490329119)
Speaker: Dr. Christopher Fell
Affiliation: Simons Postdoctoral Fellow, Abudayyeh & Gootenberg Lab, Harvard Medical School; Gene and Cell Therapy Institute, Mass General Brigham
Talk title: Repurposing natural enzymes for large genomic edits

Abstract: Treating human genetic disorders remain a large, unmet need. Gene editing technologies are rapidly advancing to clinics but are limited in the scale of edits that they can make. In this talk, I will present recent advances in the emerging gene editing modality called Programmable Gene Integration (PGI), which may be able to treat genetic diseases through gene replacement or supplementation.

SCSB Colloquium Series with Dr. Oliver Rollins: What Antiracism means for (Neuro)science Today
2025-04-30 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Wednesday, April 30, 2025
Location: 46-3002 (Singleton Auditorium)
Speaker: Oliver Rollins, Ph.D.
Affiliation: Assistant Professor of Science, Technology, and Society (STS), MIT
Hosts: Dr. Mriganka Sur, Dr. Rebecca Saxe
Talk title: What Antiracism means for (Neuro)science Today
Abstract: Historically, race—especially its erroneous interpretation as a biological reality—has played a key role in shaping scientific research about the brain. Today, neuroscience, like other related fields of biological inquiry, not only rejects its racist past but also seeks to clarify that race holds little scientific relevance in the present. In response to the Summer of 2020, for example, major scientific journals (e.g., Nature, Science, and JAMA) and institutions issued calls to better recognize and combat the underlying harms of scientific racism. However, our current sociopolitical environment raises questions about whether and how neuroscience can genuinely confront its past and contemporary interactions with race. By emphasizing how racial inequality can be perpetuated and confronted through everyday technological practices involving the brain, I aim to provide evidence of the necessity for neuroscientists and social scientists to think more collectively, critically, and creatively about the intersections between (neuro)science and the politics of social difference.

SCSB Lunch Series with Dr. Lukas Vogelsang: Temporal processing in autistic and non-autistic individuals
2025-04-18 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, April 18, 2025
Time: 12:00pm – 1:00pm
Location: Simons Center Conference room 46-6011 + Zoom (https://mit.zoom.us/j/99385139351)
Speaker: Dr. Lukas Vogelsang
Affiliation: Simons Postdoctoral Fellow, Pawan Sinha Lab, Department of Brain and Cognitive Sciences, MIT
Talk title: Temporal processing in autistic and non-autistic individuals
Abstract: Every developing nervous system confronts its own version of what William James famously described as “one great blooming, buzzing confusion”. Transforming sensory experience into a sensorium of meaningful entities and their inter-relationships lies at the core of perceptual organization. In this talk, I argue that a powerful key to understanding this process may lie in the temporal structure of the sensory environment. I will describe experiments aimed at behaviorally assessing temporal processing in both typical and atypical development, including in autistic individuals. Collectively, these investigations may illuminate temporal processing mechanisms and can help advance our understanding of sensory processing in autism.
Click to view talk recording

SCSB Lunch Series with Dr. Amrita Lamba: Neurocomputational mechanisms of disordered social interaction
2025-03-21 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, March 21, 2025
Time: 12:00pm – 1:00pm
Location: Simons Center Conference room 46-6011 + Zoom (https://mit.zoom.us/j/92058835886)
Speaker: Dr. Amrita Lamba
Affiliation: Simons Postdoctoral Fellow, Rebecca Saxe Lab, Department of Brain and Cognitive Sciences, MIT
Talk title: Neurocomputational mechanisms of disordered social interaction

Abstract: A core mission of computational psychiatry is to identify latent cognitive and neural dimensions underlying distinct phenotypic expressions of psychopathology—put simply, symptom profiles with a shared clinical label may not necessarily arise from a common underlying pathology. This heterogeneity in presentation, and possibly in underlying mechanism, presents a major hurdle for implementing effective and scalable interventions. In this talk, I will discuss how behavior in social interactions can help dissociate anxiety disorders, the leading clinical diagnosis in the United States and one of the most common comorbid diagnoses with autism spectrum disorders. I will first present data showing that processing uncertainty, causal attribution, and navigating social tension are core social cognitive dimensions that 1) shape social behavior and 2) individuals in the general population drastically vary along. I will then show that these dimensions can be simultaneously measured by combining computational models with economic games designed to elicit naturalistic social behavior. Using the Asymmetric Social Exchange (ASE) game, an economic game where participants actively manage uncertainty and social tension, I then show that social and generalized anxiety can be behaviorally dissociated in social interaction. Specifically, I will show evidence of a double dissociation in which social anxiety is associated with reduced expression of social preferences and more precisely tailoring one’s behavior to a partner. These behavioral patterns are well-captured by a Bayesian Reinforcement Learning model that produces more conformist, conflict-avoidant behavior. In contrast, generalized anxiety is associated with reduced uncertainty processing and increased aversive generalization, a pattern captured by the same model, which produces rigid and inflexible behavior. I will then present plans for future work to study the neural basis of social interaction with fMRI, potentially providing a window into dissociable neural pathways underlying social and generalized anxiety disorders.
_____________________________
Biosketch/CV: Amrita earned her B.Sc. in Psychology & Neuroscience from the University of Toronto and received her M.A. from William & Mary. During her doctoral training at Brown University, Amrita integrated social neuroscience with Reinforcement Learning and Bayesian Inference models to examine how humans learn about the statistics of their social world. Using this approach, Amrita’s Ph.D. work identified altered social learning mechanisms in people with generalized anxiety.
Website Link: https://www.amritalamba.com/

SCSB Colloquium Series with Helen Tager-Flusberg: Rethinking the Place of Language in Autism Spectrum Disorder
2025-03-19 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Wednesday, March 19, 2025
Location: 46-3002 (Singleton Auditorium)
Speaker: Helen Tager-Flusberg, Ph.D.
Affiliation: Professor Emerita, Department of Psychological & Brain Sciences, Boston University
Hosts: Dr. Mriganka Sur, Dr. Ev Fedorenko
Talk title: Rethinking the Place of Language in Autism Spectrum Disorder
Abstract: Historically, deficits in language were among the defining characteristics of ASD, however they were eliminated in DSM 5 over a decade ago. This change reflected shifts in who was being diagnosed with ASD, including increasing numbers of verbally fluent individuals, as well as individuals with genetic syndromes, many of whom are non- or minimally-verbal. In this talk, I will survey developmental, psycholinguistic and neuroimaging research with the goal of identifying the nature of language/communication impairments, if any, that cross the full spectrum of ASD. Many factors contribute to the range of differences in language in ASD from sensory and motor; cognitive and linguistic but here, I propose that one unifying difference is in the structure and functioning of the speech-motor system. Discussion will then focus on evidence for this proposal as well as implications for advancing biological studies and informing treatment research.

SCSB Colloquium Series with Dr. Haitham Amal: The NO Answer for Autism Spectrum Disorder
2025-03-05 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Wednesday, March 5, 2025
Location: 46-3002 (Singleton Auditorium)
Speaker: Haitham Amal, PhD
Affiliation: Associate Professor (Tenured), The School of Pharmacy, Faculty of Medicine, Hebrew University of Jerusalem; Visiting Professor, Boston Children’s Hospital, Harvard Medical School, Harvard University
Host: Dr. Alan Jasanoff
Talk title: The NO Answer for Autism Spectrum Disorder
Abstract: Autism spectrum disorder (ASD) is a neurodevelopmental disorder that shares core behavioral deficits. A few molecular mechanisms have been identified in ASD when most of the studies focus on a single pathway/target. To date, no effective single-drug treatment has been found for ASD, which raises the need for new drug targets. We hypothesize that multi-molecular pathways parallelly may lead to synaptic/neuronal dysfunctions and eventually to ASD phenotype. Our multi-proteomic approach using clinical and mouse model samples identified three novel potential targets possibly orchestrating in ASD: (1) de novo S-nitrosylation (NO-mediated protein modification) of the TSC2 protein. In this talk, I will focus on the role of NO (nitric oxide) in ASD. (2) Upregulation of Gephyrin phosphorylation at specific sites, which affects synaptic plasticity and functions. (3) An abnormal upregulation of the catalytic subunit of the mitochondrial ATP synthase, which may affect the integrity of the inner mitochondrial membrane. Here, we used ASD human plasma samples, human induced pluripotent stem cells (hiPSCs), and mouse models to perform a comprehensive study of the mechanisms underlying ASD pathology. The three-way pathological mechanisms were investigated using a state-of-the-art multi-proteomics platform coupled with sophisticated systems biology analyses to filter out ASD-relevant molecular changes. Pharmacological and CRISPR/Cas9 tools were used to validate the targets and explore the molecular and synaptic features following interventions. Three mouse models of ASD (Shank3, Cntnap2, and Nlgn3) were used to evaluate the behavioral outcomes of the pharmacological treatment. This talk will focus on deciphering unknown multi-way molecular mechanisms underlying ASD pathology that may uncover novel drug targets for ASD.

SCSB Lunch Series with Dr. Yunjin Lee: Brain-wide mapping of immune receptors uncovers a neuro-modulatory role of interleukin-17E and the receptor IL-17RB
2025-02-28 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, February 28, 2025
Time: 12:00pm – 1:00pm
Location: Simons Center Conference room 46-6011 + Zoom (https://mit.zoom.us/j/93152386467)
Speaker: Dr. Yunjin Lee
Affiliation: Postdoctoral Researcher, Jun Huh Lab, Harvard Medical School
Talk title: Brain-wide mapping of immune receptors uncovers a neuro-modulatory role of interleukin-17E and the receptor IL-17RB
Abstract: Cytokines and their receptors regulate diverse processes, including immune responses and behavior. Our brain-wide mapping of IL-17 receptor subunits revealed that IL-17RB expression in the cortex plays a key role in modulating social behaviors. We further demonstrated that IL-17E, acting on IL-17RB-expressing cortical neurons, enhances social interaction, highlighting a novel neuro-immune circuit that links cytokine signaling to behavioral outcomes.

SCSB Lunch Series with Dr. Emalie McMahon: The computational basis of human social vision
2025-02-14 16:00 - 17:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, February 14, 2025
Time: 12:00pm – 1:00pm
Location: Simons Center Conference room 46-6011 + Zoom (https://mit.zoom.us/j/99342137501)
Speaker: Dr. Emalie McMahon
Affiliation: Postdoctoral Associate, Nancy Kanwisher Lab, McGovern Institute, MIT
Talk title: The computational basis of human social vision
Abstract: Understanding the social interactions of others is a fundamental human ability that relies on complex neural processes and shapes our social decisions. My work focuses on uncovering the computational mechanisms behind this process, particularly the visual basis of this ability. By combining psychology, neuroscience, and computer science, I have demonstrated how the brain organizes and processes social-visual information, particular its reliance on hierarchical spatiotemporal computations. I also explored the limitations of artificial intelligence in modeling human social perception, revealing significant gaps compared to human social perception. My research advances our understanding of how the brain perceives social interactions, informs the development of socially intelligent AI, and provides a mechanistic basis for characterizing typical and atypical development, such as autism.

SCSB Colloquium Series with Dr. Robert C. Froemke: Love, Death, and Oxytocin: The Challenges of Mouse Maternity
2025-02-05 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Wednesday, February 5, 2025
Location: 46-3002 (Singleton Auditorium)
Speaker: Robert C. Froemke, PhD
Affiliation: Skirball Professor of Genetics, Neuroscience Institute and Department of Otolaryngology, NYU Grossman School of Medicine
Hosts: Dr. Mriganka Sur, Dr. Rawan AlSubaie
Talk title: Love, Death, and Oxytocin: The Challenges of Mouse Maternity
Abstract: The neuropeptide oxytocin is important for maternal physiology and social behavior. I will discuss new and unpublished data from our lab on when, where, and how oxytocin is released from hypothalamic neurons to enable maternal behavior in new mother mice. I will focus on maternal responses to infant distress calls, and how oxytocin enables rapid neurobehavioral changes for dams and alloparents to recognize the meaning of these calls. We have built a new system combining 24/7 continuous video monitoring with neural recordings from the auditory cortex and oxytocin neurons of the hypothalamus in vivo. With this documentary approach, we have identified behaviors of experienced and naïve adults learning to co-parent together which also activate oxytocin neurons. I will discuss circuits routing sensory information to oxytocin neurons leading to oxytocin release in target areas important for maternal motivation, and new results on how oxytocin controls gestation and parturition. Finally, I will discuss longer-term behavioral monitoring over months, examining how single mothers build nests to help ensure pup survival or how this sometimes goes awry.

SCSB Colloquium Series with Dr. Katalin M. Gothard: Interoceptive signals bias perception and decision making
2024-12-11 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Wednesday, December 11, 2024
Location: 46-3002 (Singleton Auditorium)
Speaker: Katalin M. Gothard, M.D., Ph.D.
Affiliation: Professor of Physiology, College of Medicine, The University of Arizona
Host: Dr. Mehrdad Jazayeri
Talk title: Interoceptive signals bias perception and decision making
Abstract: Grooming by a trusted social partner represents the macaque equivalent of affective touch in humans. In both species, affective touch induces vagal tone, a hallmark of positive affect. In this socio-emotional context, instead of responding to each sweep, neurons in the amygdala respond to a bout of grooming with small but sustained alterations in baseline firing rates. We hypothesize that these small but consistent baseline changes are driven by interoceptive afferents signaling the body’s physiological state to the brain as part of the coordinated brain-body state of positive affect. To test this hypothesis, we manipulated the physiological state of the body using drugs with minimal or no direct effect on the brain and measured the resulting changes in the spontaneous activity of neurons in the brain. We observed a clear correlation between heart rate and baseline neuronal firing rates in the amygdala and somatosensory areas, suggesting that the spontaneous neural activity closely tracks fluctuations in internal physiological states. To determine the putative cognitive and behavioral consequence of different body states we measured the changes in decision making induced by the drugs that altered baseline firing rates. Monkeys performed an approach-avoidance conflict task, where they had the option to either endure a mildly aversive (but not painful) stimulus in exchange for juice reward or to end the trial by terminating both the aversive stimulus and the reward. Drug-induced sympathetic-dominated states reduced the monkeys’ tolerance for aversive stimuli, indicating a causal relationship between physiological states and decision-making. Ongoing studies explore where and how interoceptive afferents bias decision making in the brain.

SCSB Lunch Series with Dr. Francisco Garcia: Distinct glio-vascular interactions and contributions to cerebrovascular function
2024-12-06 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, December 6, 2024
Time: 12:00pm – 1:00pm
Location: Simons Center Conference room 46-6011 + Zoom (https://mit.zoom.us/j/92275778173)
Speaker: Dr. Francisco Garcia
Affiliation: Postdoctoral Associate, Myriam Heiman Lab, PILM, MIT
Talk title: Distinct glio-vascular interactions and contributions to cerebrovascular function
Abstract: With advances in single cell technologies, it is now possible to define molecular profiles for distinct populations of cells in the brain. However, cells that comprise the cerebrovasculature have been historically difficult to capture until recently. In our work, we have developed methods for capturing cerebrovascular cell types for single-nucleus RNA sequencing (snRNA-seq) from both mouse and human brains. In doing so, we have identified a subpopulation of astrocytes that exhibits a distinct gene expression signature more closely associated with vascular function. In this seminar, I will discuss our on-going efforts to characterize these vasculature-coupled astrocytes (vc-astrocytes) in both mice and humans as well as their possible roles in brain homeostasis.

Autism and Neurodevelopmental Disorders: Past, Present, and Future
2024-11-15 14:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States

SCSB Colloquium Series with Dr. Elizabeth V. Goldfarb: Insights into multiple memory processes through studying stress and drinking
2024-11-13 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Wednesday, November 13, 2024
Location: 46-3002 (Singleton Auditorium)
Speaker: Elizabeth V. Goldfarb, Ph.D.
Affiliation: Assistant Professor of Psychiatry and of Psychology, Yale University
Host: Dr. Ev Fedorenko
Talk title: Insights into multiple memory processes through studying stress and drinking
Abstract: We remember our experiences in many different ways, varying in detail, integration, and flexibility. In this talk, I will discuss work from my lab examining how stress and drinking transform our memories, and the consequences of memory for later choices. Using new behavioral tasks and neuroimaging methods, I address questions including: what kinds of memories are prioritized following stress or trauma? How do stress and alcohol history make certain memories stronger? What are the consequences of memory biases for experiment-based decisions and real-world behavior? In answering these questions, I highlight inspiration from tasks developed in nonhuman animal models, and how memory processes can provide a bridge to translate insights across species and disorders. This work uncovers consequential and dynamic interactions between affect and our multifaceted memories.

SCSB Lunch Series with Earl Miller: Understanding and mitigating sensory overload
2024-11-08 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, November 8, 2024
Time: 12:00pm – 1:00pm
Location: Simons Center Conference room 46-6011 + Zoom [https://mit.zoom.us/j/98092241987]
Speaker: Earl K. Miller, Ph.D.
Affiliation: Picower Professor of Neuroscience, Picower Institute for Learning and Memory, MIT
Talk title: Understanding and mitigating sensory overload
Abstract: Our research indicates that brain waves serve distinct functions. High-frequency waves carry sensory data, while low-frequency waves act as control signals. The interplay between these waves regulates sensory processing and control mechanisms. Imbalances in this system may contribute to neuropsychiatric disorders. Excessive high-frequency activity could lead to attention issues or sensory overload, while insufficient high-frequency activity might be linked to psychosis. We’re working to understand the role of brain waves and how balancing them could provide treatments for various neuropsychiatric conditions.

Special Seminar with Dr. Jacque Pak Kan Ip: Functional and Molecular Dissection of Cortical Visual Impairment in CDKL5 Deficiency Disorder
2024-11-01 12:00 - 13:00 | Simons Center Conference Room, Bldg. 46, Room 6011, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Friday, November 1, 2024
Location: Simons Center Conference room, 46-6011 + Zoom [https://mit.zoom.us/j/99250543803]
Speaker: Jacque Pak Kan Ip, Ph.D.
Affiliation: School of Biomedical Sciences, Gerald Choa Neuroscience Institute, The Chinese University of Hong Kong
Host: Dr. Mriganka Sur
Talk title: Functional and Molecular Dissection of Cortical Visual Impairment in CDKL5 Deficiency Disorder
Abstract: CDKL5 deficiency disorder (CDD) is a neurodevelopmental disorder linked to the X chromosome and caused by genetic deficits in Cyclin Dependent Kinase-like 5 (CDKL5). Initially categorized as the early-onset-seizure variant of Rett syndrome, CDD is now recognized as a distinct condition with its own ICD-10 code (G40.42) assigned by the World Health Organization. However, CDD remains relatively understudied compared to other X-linked neurodevelopmental disorders such as Rett syndrome and Fragile X syndrome. Individuals with CDD experience a range of symptoms, including global developmental delay, motor dysfunction, early-onset epilepsy, learning disabilities, and autistic features. Notably, cortical visual impairment is a common clinical feature observed in at least 75% of CDD patients. Although cortical visual impairment has been suggested as a potential functional biomarker, the developmental and specific mechanisms underlying sensory processing impairments caused by CDKL5 deficits are not well understood. CDKL5 is a serine/threonine kinase, and several substrates have been identified. While research has provided insights into its molecular and cellular functions of CDKL5, its direct connection to the microcircuit development and cortical visual impairment seen in CDD is yet to be established. To address this, our study utilizes a CDD mouse model and employs in vivo two-photon calcium imaging to investigate how CDKL5 deficiency in the primary visual cortex (V1) contribute to developmental and functional deficits. Our findings reveal that Cdkl5 mutant mice exhibit impaired orientation selectivity, binocular integration, decreased neural signal amplitude, reduced neural coding ability, and network dysfunction, as observed through in vivo two-photon calcium imaging. Through a phospho-proteomics screen, we identify novel CDKL5 substrates. We further demonstrate that the absence of CDKL5 phosphorylation on the novel substrates leads to abnormal formation of RNA granules by affecting the dynamic process of liquid-liquid phase separation. Notably, deficits in the phosphorylation of the substrates alone are sufficient to induce cortical visual impairment similar to that observed in CDD. In summary, our study highlights circuit-specific cortical impairments in a CDD mouse model and uncovers a novel mechanism involving CDKL5. These findings provide insights into potential therapeutic strategies for CDD and shed light on the understanding of this complex neurodevelopmental disorder.

SCSB Colloquium Series with Dr. Yang Zhou: A Role of ASD-associated CHD8 in Reactive Gliosis and Neuroinflammation in the Adult Brain
2024-10-30 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Date: Wednesday, October 30, 2024
Location: 46-3002 (Singleton Auditorium)
Speaker: Yang Zhou, Ph.D.
Affiliation: Assistant Professor, Montreal Neurological Institute, McGill University
Host: Dr. Robert Desimone

Talk title: A Role of ASD-associated CHD8 in Reactive Gliosis and Neuroinflammation in the Adult Brain
Abstract: Mutation of genes encoding synaptic proteins and chromatin remodeling factors represents two categories of risk genes for ASD and neurodevelopmental disorders. Understanding gene function and modeling diseases with relevant mutations constitute substantial tasks in fundamental neuroscience. While encouraging progress has been made in deciphering synaptic gene mutation and modeling associated NDDs, there remains much to do and learn about chromatin remodeling factors. In this talk, I would like to share our study on the function and mechanisms of an ASD-associated chromatin factor (CHD8) in gliosis and neuroinflammation. Given that excessive reactive gliosis and neuroinflammation are hallmark features in neurodegeneration and brain injury. I will introduce ongoing efforts and discuss the potential of targeting CHD8 for alleviating neuroinflammation and brain pathophysiology in experimental models of neurological disorders.

SCSB Colloquium Series with Dr. Michael J Frank: From Descriptive to Normative Accounts of Frontostriatal Control
2024-10-16 16:00 - 17:00 | Singleton Auditorium, Bldg. 46, Room 3002, 43 Vassar Street, Cambridge, MA, 02139, United States
Michael Frank Edgar L. Marston Professor of Psychology, Director of the Center for Computational Brain Science
Date: Wednesday, October 16, 2024
Location: 46-3002 (Singleton Auditorium)
Speaker: Michael J Frank, Ph.D.
Affiliation: Edgar L Marston Professor of Cognitive & Psychological Sciences; Professor of Brain Science; Director Carney Center for Computational Brain Science, Brown University
Host: Dr. Ann Graybiel
Talk title: From Descriptive to Normative Accounts of Frontostriatal Control
Abstract: The basal ganglia and dopaminergic (DA) systems are well studied for their roles in reinforcement learning, but the underlying architecture is notoriously complex. First, I will present a computational account of how this complexity is optimized to provide robust advantages over traditional reinforcement learning models over a range of environments, and suggest that empirical observations of altered learning and decision making in patient populations reflect a byproduct of an otherwise normative mechanism. Second, I will show how this system, when interacting with prefrontal cortex, can learn to influence cognitive actions such as working memory updating and “chunking” strategies that are adapted as function of task demands, mimicking human performance and normative models.
