SFARI

SFARI Society for Neuroscience 2017 Social
2017-11-13 18:30 - 20:30 UTC | Marriott Marquis Washington, D.C. Liberty Salons I, J, K, 901 Massachusetts Ave NW, Washington, D.C., 20001, United States
All Society for Neuroscience (SfN) attendees are welcome to join SFARI Investigators and scientific staff for an evening of socializing and networking, including a brief information session on SFARI funding opportunities and scientific resources for the autism research community.
We welcome newcomers to autism research as well as those already working to uncover the science of autism spectrum disorders.
Simons Foundation staff will be available to answer questions about the work SFARI currently funds, future opportunities for funding and SFARI resources.

A number of SFARI Investigators will be presenting their research at Neuroscience 2016.To find out more, click here.

SFARI + SfN Social
Date: Monday, 13 November 2017
Time: 6:30 p.m. – 8:30 p.m.
Marriott Marquis Washington, D.C.
Liberty Salons I, J, K
Questions? Contact communications@simonsfoundation.org.
We look forward to seeing you there.

Understanding autism and other neurodevelopmental disorders: From the embryo to brain organoids
2017-11-01 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States

Leveraging long-term health data and exome sequencing for autism-related gene discovery
2017-10-11 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States

What can genetics tell us about autism spectrum disorder?
2017-03-22 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 22 March 2017, Stephan Sanders presented an update on the current state of genetics research in autism, highlighting some of the key findings that remain to be discovered, and discussing how these findings could ultimately benefit individuals with autism and their families.
His talk was part of the Simons Foundation Autism Research lecture series.
About the Lecture
It has been known that autism spectrum disorder is primarily caused by genetic factors for several decades. The past 10 years have seen great progress in finding some of the genes responsible and in building a map of what other types of genetic variants may contribute. These findings have been used both to provide insight into the biology of autism and, in the clinic, to identify individuals with specific genetic variants.
In this lecture, Stephan Sanders presented an update on the current state of genetics research in autism, highlight some of the key findings that remain to be discovered, and discussing how these findings could ultimately benefit individuals with autism and their families.
About the speaker:
Stephan Sanders trained as a pediatric physician in the United Kingdom before pursuing a research career in genomics and bioinformatics. His work has helped characterize the role of de novo mutations in the etiology of autism and identified multiple autism risk loci, including duplications of the 7q11.23 Williams syndrome region (Sanders et al., Neuron, 2011) and mutations in the sodium channel gene SCN2A (Sanders et al., Nature, 2012). His work on the integration of copy number variation and exome data across multiple autism cohorts recently identified 71 autism risk loci (Sanders et al., Neuron, 2015). In addition, he worked as part of a group that integrated spatiotemporal gene expression data from the human brain with these autism-associated genes (Willsey et al., Cell, 2013). This approach has implicated deep-layer glutamatergic neurons in the frontal cortex during mid-fetal development in the causation of autism.
His lab has three main research aims: 1) Understanding the genetic basis of childhood neurodevelopmental conditions, in particular autism; 2) Understanding how these genetic factors lead to the conditions; and 3) Understanding the mechanism that leads to the male bias in autism diagnosis, in particular through identifying the biological basis of the female protective effect.

Exploiting genetics to identify environmental risks for autism
2017-02-22 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 22 February 2017, Mark Zylka described how candidate environmental risk factors for autism can be identified rationally, by pinpointing chemicals that interfere with the same molecular pathways that are affected in individuals with autism.
His talk was part of the Simons Foundation Autism Research lecture series.
About the Lecture
Our inability to identify environmental threats to the brain early — before they cause disease — represents one of the major challenges of our time. This challenge is particularly relevant to autism, which affects 1 in 68 individuals. Heritability studies indicate that environmental factors contribute to autism risk.
In this lecture, Mark Zylka described how candidate environmental risk factors for autism can be identified rationally, by pinpointing chemicals that interfere with the same molecular pathways that are affected in individuals with autism. His research focuses on identifying environmental-use chemicals that target autism-linked molecular pathways, using environmental sampling data to assess the exposure threat to people, and validating risk potential in animal models.
About the speaker:
Mark Zylka is Director of the Neuroscience Center at the University of North Carolina at Chapel Hill. He received his B.S. in biochemistry from Virginia Polytechnic Institute and State University, and his Ph.D. in neurobiology from Harvard University. While at Harvard, he identified several of the core circadian-clock genes and determined how these genes contribute to circadian rhythms in mammals. As a postdoctoral fellow at the California Institute of Technology, he identified a large family of receptors that regulate pain and itch. Zylka’s lab focuses on pain research and studying genetic and environmental risks for autism.

Genomic insights into human cortical development and neurodevelopmental disease
2017-02-01 17:00 - 18:00 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States

Potholes and progress on the road to translational treatments in autism spectrum disorder
2017-01-25 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 25 January 2017, Jeremy Veenstra-VanderWeele outlined critical challenges to translating genomic, cellular, and animal model research into new treatments for autism spectrum disorder.
His talk was part of the Simons Foundation Autism Research lecture series.
About the Lecture
Emerging genomic and neuroscience findings have delivered hypotheses that are now being tested in autism spectrum disorder (ASD) and related genetic syndromes. Unfortunately, these clinical trials have not yet yielded positive results, suggesting a need to step back and evaluate the science of testing new treatments for neurodevelopmental disorders.
In this lecture, Jeremy Veenstra-VanderWeele outlined critical challenges, both conceptual and practical, to translating genomic, cellular, and animal model research into new treatments for ASD. He discussed the limitations to conclusions drawn from work in the laboratory as they are extrapolated to the clinic. He also described common pitfalls in clinical trials, including mismatches between hypotheses and study populations, substantial “placebo” effects, and subjective outcome measures. Framing these challenges in the context of past successes in ASD treatment research, he suggested guideposts as we work toward neurobiologically based treatments for ASD.
About the speaker:
Jeremy Veenstra-VanderWeele is the Mortimer D. Sackler, M.D., Associate Professor in Psychiatry at Columbia University Medical Center and the New York State Psychiatric Institute. He completed his M.D. and residency training at the University of Chicago, postdoctoral training in neuroscience at Vanderbilt University, and moved to Columbia in 2014. As a child psychiatrist and developmental neuroscientist, his primary motivation is to deliver new treatments to children with autism spectrum disorder and related neurodevelopmental disorders.

SFARI Society for Neuroscience 2016 Social
2016-11-14 18:30 - 20:30 | Hilton San Diego Bayfront Indigo 204, One Park Blvd, San Diego, CA, 92101, United States
All Society for Neuroscience (SfN) attendees are welcome to join SFARI Investigators and scientific staff for an evening of socializing and networking, including a brief information session on SFARI funding opportunities and scientific resources for the autism research community.
We welcome newcomers to autism research as well as those already working to uncover the science of autism spectrum disorders.
Simons Foundation staff will be available to answer questions about the work SFARI currently funds, future opportunities for funding and SFARI resources.

A number of SFARI Investigators will be presenting their research at Neuroscience 2016.
To find out more, click here.

SFARI + SfN Social
Date: Monday, 14 November 2016
Time: 6:30 p.m. – 8:30 p.m.
Hilton San Diego Bayfront
Indigo 204
Questions? Contact communications@simonsfoundation.org.
We look forward to seeing you there.

How immune cells help wire the brain: Implications for autism and psychiatric illness
2016-11-02 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 2 November 2016, Beth Stevens discussed recent work that implicates brain immune cells, called microglia, in sculpting of synaptic connections during development and their relevance to autism, schizophrenia and other brain disorders.
Her talk was part of the Simons Foundation Autism Research lecture series.
About the Lecture
Recent research has revealed a key role for microglia and a group of immune-related molecules, called complement, in normal developmental synaptic pruning, a process required to establish precise brain wiring. Emerging evidence from Beth Stevens’ lab and others suggest aberrant regulation of this pruning pathway may contribute to synaptic and cognitive dysfunction in a host of brain disorders, including schizophrenia. Studies also suggest that a person’s risk of schizophrenia is increased if he or she inherits specific variants in complement C4, which plays a well-known role in the immune system but also helps sculpt developing synapses in the mouse visual system.
Together these findings may help explain known features of schizophrenia, including reduced numbers of synapses in key cortical regions and an adolescent age of onset that corresponds with developmentally timed waves of synaptic pruning in these regions. Stevens discussed this and ongoing work to understand the mechanisms by which complement and microglia prune specific synapses in the brain. A deeper understanding of how these immune mechanisms mediate synaptic pruning may provide novel insight into how to protect synapses in autism and other brain disorders.
About the speaker
Beth Stevens is an assistant professor of neurology at Harvard Medical School and the F.M. Kirby Neurobiology Center at Boston Children’s Hospital and a member of the Broad Institute. Her laboratory seeks to understand how neuron-glia communication facilitates the formation, elimination and plasticity of synapses during both healthy development and disease states. Stevens is a recipient of several young investigator awards, including the Ellison Medical Foundation New Scholar in Aging; John Merck Scholar Program; Presidential Early Career Award for Scientists and Engineers; and a MacArthur Fellowship.

Tuberous Sclerosis: Shedding light on the neural circuitry of autism
2016-10-05 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 5 October 2016, Mustafa Sahin presented an update on translational research in Tuberous Sclerosis Complex. His talk was part of the Simons Foundation Autism Research lecture series.
About the Lecture
In this lecture, Mustafa Sahin presented the rationale for investigating Tuberous Sclerosis Complex (TSC) as a way to understand the cellular and circuitry alterations underlying autism spectrum disorder. Using a combination of cell culture, mouse behavior and human electroencephalography (EEG) and magnetic resonance imaging (MRI) experiments, Sahin and colleagues have demonstrated abnormalities in neuronal connectivity and neuron-glia interactions in TSC. Inhibitors of mammalian target of rapamycin (mTOR) proteins are effective in mouse models of TSC and are being tested in clinical trials now. A better understanding of TSC can also provide insights for related neurodevelopmental disorders in which similar cellular and circuit abnormalities can be detected.
About the Speaker
Mustafa Sahin is a developmental neurobiologist and a pediatric neurologist. He received his B.S. degree from Brown University, his M.D. and Ph.D. from Yale School of Medicine. He completed a pediatrics residency at Children’s Hospital of Philadelphia and a child neurology residency at Boston Children’s Hospital. He is currently the director of the Translational Neuroscience Center at Boston Children’s Hospital and a professor of neurology at Harvard Medical School. He directs two national consortia to study biomarkers and comparative pathobiology of TSC and related neurodevelopmental disorders.

Sleep in autism spectrum disorders: A window to etiology, diagnosis and treatment
2016-09-07 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 7 September 2016, Ruth O’Hara discussed the field’s current understanding of sleep in autism spectrum disorder.
Her talk was part of the Simons Foundation Autism: Emerging Concepts lecture series.
About the Lecture
Understanding sleep physiology in autism spectrum disorder (ASD) not only provides a window to the underlying etiology, it can also help characterize sub-phenotypes and offer a potent treatment approach for improving neuropsychiatric and neurocognitive function in ASD through improved sleep.
Ruth O’Hara discussed the field’s current understanding of sleep in ASD, including: a) describing how sleep physiology in ASD differs from sleep physiology in typically developing children; b) discussing the different potential ASD phenotypes suggested by her work; and c) describing the different sleep architecture, sleep disturbances, and sleep disorders that are more prevalent in ASD than in typically developing children and which can serve as treatment targets that may in turn improve the core symptoms of ASD.
About the speaker:
Ruth O’Hara is associate professor and associate chair of the Department of Psychiatry at Stanford University. Her research integrates measures of sleep physiology, the brain and behavior across the lifespan. Over the years she has obtained substantial National Institutes of Health (NIH) funding to support her work. O’Hara received a SFARI grant to examine sleep physiology and neurodevelopmental processes in autism spectrum disorder. She was a member of the most recent Diagnostic and Statistical Manual of Mental Disorders (DSM) sleep-wake disorders work group.

One brain, many genomes: Somatic mutation and genomic variability in human cerebral cortex
2016-04-27 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 27 April 2016, Christopher Walsh reviewed recent work on ‘somatic mutations’ — de novo mutations that are present in some brain cells but not in all cells of the body — in several neurological conditions associated with intellectual disability and seizures.
His talk was part of the Simons Foundation Autism Research lecture series.
About the Lecture
Christopher Walsh and his team are interested in genetic mechanisms of cerebral cortical development and abnormalities of cortical development resulting in intellectual disability, autism and epilepsy. The lab pioneered the analysis of recessive causes of autism by studying children with autism whose parents share ancestry.
In this lecture, Walsh reviewed recent work on ‘somatic mutations’ — de novo mutations that are present in some brain cells but not in all cells of the body — in several neurological conditions associated with intellectual disability and seizures. His talk also covered the extent to which somatic mutations are an inevitable part of normal brain development, such that the neurons in the human brain are a tapestry of cells with distinct genomes. The relevance of somatic mutations to autism was also discussed.
About the Speaker
Christopher A. Walsh is Chief of the Division of Genetics and Genomics at Boston Children’s Hospital, Bullard Professor of Pediatrics and Neurology at Harvard Medical School, and an investigator of the Howard Hughes Medical Institute. He completed the M.D. and Ph.D. degrees at the University of Chicago, trained in neurology at Massachusetts General Hospital, and has been at Children’s Hospital since 2006.

Development begins before birth: Prenatal research relevant to autism
2016-03-30 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 30 March 2016, Catherine Monk described her lab’s fetal origins of adult disease (FOAD) studies that focus on women in the perinatal period and fetal and infant neurobehavioral development, including direct studies of the fetus, newborn brain imaging and placental methylation. Her talk was part of the Simons Foundation Autism Research lecture series.
About the Lecture
The burgeoning research field known as the fetal origins of adult disease (FOAD) or the developmental origins of health and disease (DOHAD) demonstrates that maternal distress during pregnancy affects fetal and infant brain–behavior development. This is a ‘third pathway’ for the familial inheritance of psychiatric illness beyond shared genes and the quality of parental care, and one that, if fully understood, could lead to early prevention of developmental risk.
In this lecture, Catherine Monk described her lab’s FOAD studies that focus on women in the perinatal period and fetal and infant neurobehavioral development, including direct studies of the fetus, newborn brain imaging and placental methylation.
Applying the FOAD model to autism research introduces the possibility of identifying perinatal markers for the disorder and may help advance the animal and epidemiological findings showing that prenatal maternal immune activation — often a correlate of distress — is associated with risk for the illness.
About the Speaker
Catherine Monk, Ph.D., holds a joint appointment as an associate professor in the Departments of Psychiatry, and Obstetrics & Gynecology at Columbia University Medical Center. Reflecting the interdisciplinary nature of her research, she is affiliated with two divisions in psychiatry: behavioral medicine and developmental neuroscience. She is director for research at the Women’s Program, as well as co–director of the Sackler Parent–Infant Project and of the Domestic Violence Initiative. After completing her National Institutes of Health postdoctoral fellowship in the psychobiological sciences at Columbia in 2000, Dr. Monk joined the faculty and established the Perinatal Pathways Laboratory.

Making up your mind: Interneurons in development and disease
2016-01-27 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 27 January 2016, Gordon Fishell described his investigations of the developmental and genetic origins of interneuron development. His talk was part of the Simons Foundation Autism Research lecture series.
About the Lecture
Interneurons within the brain, in the cortex and hippocampus in particular, are central for normal brain function, and conversely, dysfunction of these cell types is thought to result in developmental neurological disorders. The Fishell laboratory combines genetic and physiological approaches to examine the origins of these populations and their integration into brain circuitry.
In this lecture, Gordon Fishell described his investigations of the developmental and genetic origins of interneuron development. This process begins with their specification, during which genetic programs initiated within progenitors relegate interneurons into specific cardinal classes. Subsequent to this, neuronal activity is fundamental for both the laminar positioning as well as the dendritic and axonal arborization in at least some interneuron subtypes. Fishell’s findings suggest that sensory information complements earlier established genetic programs to shape the way interneuronal subtypes integrate into nascent cortical circuits. Importantly, many of the genes involved in the maturation of interneurons appear to also be implicated in neuropsychiatric diseases, including autism and schizophrenia.
About the Speaker
Gordon J. Fishell, Ph.D., is associate director of the NYU Neuroscience Institute, Julius Raines Professor of Neuroscience and Physiology, and director of the Graduate Program in Neuroscience and Physiology at New York University (NYU) School of Medicine. Fishell is a long-standing member of the NYU School of Medicine community, having joined the developmental genetics program in the Skirball Institute of Biomolecular Medicine in 1994. In 2006, he launched the Smilow Neuroscience Program, and in 2011 he became associate director of the then-newly-formed NYU Neuroscience Institute.

Storming the ivory tower: How to make autism interventions work in schools
2015-11-11 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 11 November 2015, David S. Mandell talked about why autism interventions rarely are implemented in community practice and why they fail to achieve the same outcomes as those observed in clinical trials.
His talk was part of the Simons Foundation Autism Research lecture series.
About the Lecture
A growing body of research shows the efficacy of interventions for children with autism. These interventions rarely make their way into community practice, however. When they do, they usually do not produce the same results as those observed in clinical trials.
In this lecture, David S. Mandell will talk about why autism interventions rarely are implemented in community practice and why they fail to achieve the same outcomes as those observed in clinical trials. He will review the policy environment for improving quality of care and evidence suggesting that recently enacted policies may be necessary but are not sufficient to improve practice. He also will present research that more directly attempts to improve quality of care and associated outcomes for children with autism.
About the Speaker
David S. Mandell, Sc.D., is associate professor of psychiatry and pediatrics at the University of Pennsylvania’s Perelman School of Medicine. The goal of his research is to improve the quality of care that individuals with autism receive in their communities. He examines the effects that different state and federal strategies to organize, finance and deliver services have on service use patterns and outcomes. He also conducts experimental studies to determine the best ways to successfully implement proven-efficacious practices in community settings.

Molecular and neural architecture of circuits underlying social behavior in the mouse
2015-10-28 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 28 October 2015, Catherine Dulac discussed the cellular and molecular architecture of neural circuits underlying instinctive social behaviors in mice. Her talk was part of the Simons Foundation Autism Research lecture series.
About the Lecture
Severe mental disorders such autism spectrum disorders, schizophrenia and major depressive disorder are characterized by profound social impairments. There is little understanding of the neural mechanisms underlying these social deficits, and efficient diagnosis and therapeutic options are lacking. Advanced molecular and genetic techniques have made the discovery of specific behavior circuits possible.
In this lecture, Catherine Dulac will discuss the cellular and molecular architecture of neural circuits underlying instinctive social behaviors of mice. She will describe her group’s recent advances in uncovering the identity of sensory neurons that detect social cues and the identity of command circuits associated with specific social responses in male and female mice.
About the Speaker
Catherine Dulac received her B.Sc. from the Ecole Normale Superieure in Paris, France, her Ph.D. from the University of Paris and was a postdoctoral fellow at Columbia University. She has been a Howard Hughes Medical Institute Investigator since 1997 and a Harvard faculty in the Department of Molecular and Cellular Biology since 1996 (Chair 2007-2013). She is a recipient of the Lounsbery, Perl-UNC Neuroscience, and Pradel Research Awards. Memberships include the National Academy of Sciences and the French Academy of Sciences, and she is a Chevalier de la Legion d’Honneur.

SFARI Society for Neuroscience 2015 Social
2015-10-19 18:30 - 20:30 | Hyatt Regency Chicago Downtown Regency Ballroom A, 151 E Upper Wacker Dr, Chicago, IL, 60601, United States
All Society for Neuroscience (SfN) attendees are welcome to join SFARI Investigators and scientific staff for an evening of socializing and networking, including a brief information session on SFARI funding programs and scientific resources for the autism research community.
We welcome newcomers to autism research as well as those already working to uncover the science of autism spectrum disorders.
Simons Foundation staff will be available to answer questions about the work SFARI currently funds, future opportunities for funding and SFARI resources.

A number of SFARI Investigators will be presenting their research at Neuroscience 2015.
To find out more, click here.

SFARI + SfN Social
Date: Monday, 19 October 2015
Time: 6:30 p.m. – 8:30 p.m.
Hyatt Regency Chicago Downtown
Regency Ballroom A
Questions? Contact communications@simonsfoundation.org.
We look forward to seeing you there.

Timing mechanisms of critical periods in brain development
2015-09-30 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 30 September 2015, Takao Hensch discussed the biological bases of critical periods in brain development. Mechanisms that open and close windows of plasticity (E/I balance and molecular brakes, respectively) have been implicated in autism, suggesting mistimed maturational processes that can be strategically rescued at the circuit level. His talk was part of the Simons Foundation Autism Research lecture series.
About the Lecture
Maturing neural circuits are dramatically shaped by the environment during windows of increased plasticity, but the timing of these ‘critical periods’ varies across brain regions, and plasticity declines with age.
Focusing on cellular/molecular mechanisms underlying these developmental trajectories, Dr. Hensch discussed specific events that control the onset and closure of critical periods. Maturation of excitatory-inhibitory (E/I) circuit balance triggers plasticity, which ends when molecular brake-like factors emerge to stabilize adult networks. Targeting specific GABA circuits using pharmacological or genetic manipulations can either accelerate or delay the onset of plasticity, and lifting the molecular brakes can reopen windows of circuit rewiring. Implications for autism spectrum disorder etiology and potential therapeutic strategies were also discussed.
About the Speaker
Takao K. Hensch is a professor of neurology and of molecular and cellular biology at Harvard University, and directs the National Institute of Mental Health’s Conte Center for Basic Mental Health Research. After studying at Harvard University, the University of Tokyo (M.P.H.), the Max Planck Institute for Brain Research (Fulbright Fellowship) and the University of California, San Francisco (Ph.D.), he helped to launch the RIKEN Brain Science Institute, serving as lab head and group director for 14 years. Honors include two Young Investigator awards from the Society for Neuroscience and a National Institutes of Health Director’s Pioneer Award. He is a member of several editorial boards, including Neuron and Frontiers in Neural Circuits, where he is chief editor.

Prevalence and trends in epidemiology of autism
2015-03-25 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 25 March 2015, Maureen Durkin discussed trends in the prevalence of autism and explored some of the reasons underlying the recent rise in autism cases. Her talk was part of the Simons Foundation Autism Research lecture series.
About the Lecture
Once considered an extremely rare childhood mental disorder, autism is now recognized as a common neurodevelopmental disability, affecting more than 1 percent of the population in the U.S. Reasons for the rise in prevalence are not fully understood, but they are likely associated with societal and cultural influences, and the expansion of the concept of autism to a spectrum disorder: autism spectrum disorder.
In this lecture, Maureen Durkin discussed trends in the prevalence of autism, focusing on the role of intellectual disability — both as a co-occurring condition with autism and in terms of using autism as a diagnostic substitute for intellectual disability. She also explored evidence of socioeconomic disparities in access to diagnostic and therapeutic services for autism, the cultural and financial barriers underlying these disparities, and the need to incorporate modern concepts of disability into the epidemiology of autism, placing emphasis not only on primary prevention of impairments but also on enhancement of functioning and social inclusion of people with the disorder.
About the Speaker
Maureen Durkin is an epidemiologist, professor of population health sciences and pediatrics, and Waisman Center investigator at the University of Wisconsin-Madison. She received her Ph.D. in anthropology from the University of Wisconsin-Madison, and her M.P.H. and Dr.P.H. degrees in epidemiology from Columbia University. She conducts studies on the epidemiology of neurodevelopmental disabilities and is currently principal investigator of the Wisconsin site of the Centers for Disease Control and Prevention’s Autism and Developmental Disabilities Monitoring Network.

Learning to move
2014-12-03 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 3 December 2014, Karen E. Adolph discussed how infants learn to generate and control their movements by adapting to environmental and social factors.Her talk, which covered ways in which a variety of external factors affect how infants learn to move, was part of SFARI’s Autism: Emerging Concepts lecture series. Adolph explained how infants adaptively learn to move rather than acquiring fixed solutions.
More about the lecture:
Basic motor skills such as looking, reaching and walking do not simply appear as the result of maturation. Rather, infants must learn to move. Learning entails discovering new forms of movements to suit the task at hand and using perceptual information to select and modify movements adaptively.
In this lecture, Karen E. Adolph discussed how infants learn to generate and control their movements by adapting to environmental and social factors. Learning to move involves more than merely lifting the limbs against gravity. Adaptive action requires that movements be constructed, selected and modified in accordance with the constraints and opportunities provided by the physical and social environment. The learning process is geared toward flexibility rather than rote performance: Infants are learning to move rather than acquiring fixed solutions.
Commentator Cole Galloway provided post-lecture commentary that highlighted how mobility and socialization affect the lives of infants with special needs and their families. Galloway is director of the Pediatric Mobility Lab and Design Studio, and professor of physical therapy at the University of Delaware. Galloway began focusing on young children following a postdoctoral fellowship with Esther Thelen. His research focuses on how multiple biological, psychological and environmental factors contribute to the emergence of exploratory behaviors. Current projects focus on advancing the technology and training to assist children in maximizing their daily exploration.
About the speaker:
Karen E. Adolph is professor of psychology at the Center for Neural Science at New York University, as well as a fellow of the American Psychological Association and the Association for Psychological Science. She is incoming president of the International Society on Infant Studies and is leading the Databrary.org project to enable open sharing of video data among developmental scientists.
Adolph has pioneered research on motor skill acquisition in infants, in particular on how infants learn to use perceptual and social information to guide actions adaptively. Her research also examines the effects of body growth, exploratory activity, environmental and social supports and culture on perceptual motor learning and development.

Microbiota and the host immune system in autism
2014-10-29 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 29 October 2014, Dan Littman described how intestinal bacteria affect immune system cell functioning, potentially contributing to systemic inflammation and autism.
His talk was part of SFARI’s Autism: Emerging Concepts lecture series.
About the lecture:
Our immune system is heavily influenced by microbiota — the microbes that reside within us. In the intestine, specific microbes induce pro- or anti-inflammatory white blood cells called lymphocytes that maintain a healthy homeostasis. An imbalance of microbiota can result in dysregulated immune cells that contribute to autoimmunity and autism.
In this lecture, Dan Littman described how intestinal bacteria shape the part of the immune system that prevents invasion by harmful microbes, but they can also contribute to systemic inflammation. The bacteria regulate Th17 cells, which participate in multiple autoimmune diseases. These cells play a key role in the maternal immune activation model of autism. Activation of the pregnant mother’s innate immune response may result in lifelong behavioral defects in the child. Through this lens, Littman discussed implications for preventing or treating autism.
About the speaker:
Dan Littman earned his M.D. and Ph.D. from Washington University in St. Louis, completing a postdoctoral fellowship with Richard Axel at Columbia University. From Columbia, he moved to the University of California, San Francisco, where he was professor of microbiology and immunology. Littman is now the Helen L. and Martin S. Kimmel Professor of Molecular Immunology at the Skirball Institute of Biomolecular Medicine at New York University and an investigator at the Howard Hughes Medical Institute.

The social brain: Understanding autism
2014-09-23 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 23 September, Nancy Kanwisher discussed the functional architecture of the social brain as an avenue for considering which functions are affected and which are preserved in autism.Her talk was part of SFARI’s Autism: Emerging Concepts lecture series.
About the lecture:
Humans are a highly social species, allocating numerous brain regions to distinct aspects of social cognition. These regions and corresponding mental abilities serve as tools for understanding which functions are lost and which are preserved in autism.
Autism is characterized by a highly uneven cognitive profile in which some mental functions are preserved or enhanced, and others are disrupted. An important asset in the search to understand this complex disorder comes from the study of the typical human mind and brain.
In this talk, Nancy Kanwisher considered the functional architecture of the social brain as an avenue for considering which functions are affected and which are preserved in autism.
About the Speaker
Nancy Kanwisher is professor of cognitive neuroscience at the Massachusetts Institute of Technology (MIT) and an investigator at MIT’s McGovern Institute for Brain Research. After receiving her B.S. and Ph.D. from MIT, Kanwisher served on the faculty at the University of California, Los Angeles and Harvard University before returning to MIT in 1997. Kanwisher has received the Troland Research Award, MacVicar Faculty Fellow teaching award and Golden Brain Award. She is a member of the National Academy of Sciences and the American Academy of Arts and Sciences.

New approaches to treating Rett syndrome
2014-04-23 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 23 April, Gail Mandel presented the complex pathology of Rett syndrome and discussed whether this autism-related disorder would be amenable to gene replacement strategies. Her talk was part of the Simons Foundation Autism Research lecture series. You can watch a complete video recording of the event above.
About the Lecture
A central goal in neuroscience is determining the genetic basis of neurological disorders — from autism to brain tumors. Many of these pathological states result from defects in gene regulatory programs that are fundamental to all cell types but lead to dysfunction specifically within the nervous system. Mandel investigates the basis of this phenomenon and has identified cell-cell interactions between neurons and glia — brain cells that support neurons and help process information — involved in brain development.
Mandel has been able to treat the brain pathology of one autism-related disorder, Rett syndrome, by genetically replacing the defective MeCP2 gene with a good copy of the gene in astrocytes — a type of glia. She is exploring the underlying mechanisms crucial for neuronal signaling.
About the speaker:
Gail Mandel holds a Ph.D. in immunology from the University of California, Los Angeles, and did postdoctoral work in biochemistry and molecular biology there and at the University of California, San Diego, and Harvard Medical School. She began her career at Tufts Medical School, where she was one of the first investigators to clone and express mammalian voltage-dependent ion channels. In the department of neurobiology and behavior at Stony Brook University, she identified the protein REST, which is responsible for regulation of sodium channel expression and the acquisition of cellular excitability. These discoveries have helped unlock the mechanisms through which embryonic cell types differentiate specifically into neurons. Mandel is a senior scientist in the Vollum Institute at Oregon Health & Science University. She is an Investigator of the Howard Hughes Medical Institute and a member of the American Academy of Sciences and the National Academy of Sciences.

An attempt at redefining autism
2014-03-26 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 26 March, Ami Klin presented data from two studies measuring social adaptive behaviors — highly conserved and early-emerging mechanisms of socialization — in infants and toddlers.His talk is part of SFARI’s Autism: Emerging Concepts lecture series. You can watch a complete video recording of the event above.
About the lecture:
Advances in molecular genetics have implicated a number of genetic variants in autism, yet understanding of how these variants contribute to the disorder is limited. Autism is among the most reliably diagnosed neurodevelopmental disorders, but symptoms used to define autism are likely to be outcomes of disruptions much earlier in development. Klin’s findings might allow researchers to detect underlying characteristics associated with autism before the current average age of diagnosis.
About the speaker:
Ami Klin is Georgia Research Alliance Eminent Scholar Professor and director of the division of autism and developmental disabilities at Emory University School of Medicine. He earned his Ph.D. from the University of London and completed clinical and research work at Yale University’s Child Study Center. Until 2010, he directed the autism program at the Yale Child Study Center, and was Harris Professor of Child Psychology and Psychiatry there.
Klin’s primary research focuses on the social mind and brain and on the developmental aspects of autism from infancy through adulthood. He is the author of more than 180 publications in the field of autism and related conditions and the co-editor of Asperger Syndrome, Autism Spectrum Disorders in Infants and Toddlers, the third edition of the Handbook of Autism and Pervasive Developmental Disorders and several special issues of professional journals focused on autism.

Imaging early brain development in autism
2014-02-26 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 26 February, David Amaral presented evidence supporting the concept that there are different types of altered brain development among children with autism.His talk is part of SFARI’s Autism: Emerging Concepts lecture series. You can watch a complete video recording of the event above.
About the lecture:
Autism clearly involves altered function of the central nervous system, but the neuropathology of the disorder remains controversial. This is due in part to the enormous complexity of the disorder, with many possible causes and biological trajectories. What’s more, few neuroimaging studies involve young children or severely affected individuals. This lack of information is compounded by the fact that findings from magnetic resonance imaging cannot be confirmed and extended to the cellular level because of a lack of postmortem brains.
About the speaker:
David Amaral joined the University of California, Davis, in 1995 as a professor in the department of psychiatry and behavioral sciences and the Center for Neuroscience. He is a staff scientist in the Brain, Mind and Behavior Unit at the California National Primate Research Center. Amaral was named the Beneto Foundation Chair and research director of the MIND Institute in 1998. He received a joint Ph.D. in psychology and neurobiology from the University of Rochester.
Amaral’s research focuses on the neurobiology of social behavior and the development and neuroanatomical organization and plasticity of the primate and human amygdala and hippocampus. Increasingly, his research has been dedicated to understanding the biological basis of autism. As research director of the MIND Institute, Amaral coordinates a comprehensive and multidisciplinary analysis of children with autism, called the Autism Phenome Project, which aims to define biomedical characteristics of different types of autism.
Most recently, Amaral became director of Autism BrainNet, a collaborative effort sponsored by the Simons Foundation Autism Research Initiative and Autism Speaks. The new project aims to solicit postmortem brain tissue to facilitate autism research.

Infants' grasp of others' intentions
2013-11-06 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 6 November 2013, Amanda Woodward discussed the origins of children’s social understanding and how this fundamental aspect of cognition has profound implications for early childhood development. The talk is part of SFARI’s Autism: Emerging Concepts lecture series.
Kevin Pelphrey provided post-lecture commentary on how our growing understanding of the origins of children’s social cognition can inform the search for early diagnostic indicators of autism.
You can watch a complete video recording of the event above. Use the comments section below to discuss the lecture and pose follow-up questions.
About the lecture:
Growing evidence shows that in typical development, the ability to carry out actions according to intentions emerges during infancy. Studies over the past few years have shown that this ability develops and changes rapidly during infancy. An infant’s active engagement with the physical and social world is critical for acquiring social skills.
About the speaker:
Amanda Woodward is William S. Gray Professor of Psychology at the University of Chicago and director of the university’s Infant Learning and Development Laboratory.
Woodward is a fellow of the American Psychological Association and of the Association for Psychological Science. She is incoming president of the Cognitive Development Society and serves on the executive board of the International Society on Infant Studies. Woodward has pioneered the study of infant social cognition, particularly infants’ understanding of others’ actions and the relationship between infants’ own actions and their action perception. Her team also investigates infants’ learning from social partners, and cross-cultural variations in early social learning.
About the commentator:
Kevin Pelphrey is Harris Professor at the Yale Child Study Center and director of the Center for Translational Developmental Neuroscience and the Yale Center for Excellence in Autism Research and Treatment. As a SFARI Investigator, his research focuses on the application of cognitive neuroscience and genetics techniques to understanding the systems biology of neurodevelopmental disorders.

Evolving perspectives on autism
2013-09-26 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 26 September 2013, Catherine Lord and Steven Hyman presented conceptual frameworks for autism diagnosis and research, ranging from genetics to symptomatology, as part of SFARI’s Autism: Emerging Concepts lecture series.
Eric London provided post-lecture commentary, placing the discussion in a clinical context and providing a physician’s perspective.
You can watch a complete video recording of the event above. Use the comments section below to discuss the lecture and pose follow-up questions.
About the lecture:
Tremendous progress has been made in our understanding of autism, with major contributions coming from a variety of research fields, including genetics, neuroscience and psychology. The clinical definition of autism has been revamped with the publication of the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders. Accordingly, our concept of autism is evolving, which in turn affects the future of autism research and the development of interventions.
About the speakers:
Catherine Lord is director of the Center for Autism and the Developing Brain, a joint project of New York-Presbyterian Hospital, Weill Cornell Medical College and Columbia University College of Physicians and Surgeons in partnership with New York Collaborates for Autism.
Lord is a licensed clinical psychologist with specialties in diagnosis, social and communication development, and intervention in autism. Renowned for her work in longitudinal studies of social and communicative development in autism, Lord has also contributed to the development of diagnostic instruments for autism that are now used as global research standards.
Steven Hyman is director of the Stanley Center for Psychiatric Research at the Broad Institute of the Massachusetts Institute of Technology and Harvard University, and is Distinguished Service Professor of stem cell and regenerative biology at Harvard.
From 1996 to 2001, Hyman served as director of the U.S. National Institute of Mental Health, where he emphasized investment in neuroscience and emerging genetic technologies and initiated a series of large practical clinical trials to inform practice. He is editor of the Annual Review of Neuroscience, president-elect of the Society for Neuroscience, founding president of the International Neuroethics Society and a member of the Institute of Medicine of the U.S. National Academies.
About the commentators:
Gerald D. Fischbach is chief scientist and fellow of the Simons Foundation.
Eric London is director of the Autism Treatment Laboratory at the New York State Institute for Basic Research in Developmental Disabilities.

Antibodies, behavior and cognition
2013-05-30 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 30 May, Betty Diamond discussed how the immune system can mediate alterations in brain development and play a role in autism, as part of SFARI’s Autism: Emerging Concepts lecture series.
Alan Brown provided a post-lecture commentary and context for Diamond’s work on epidemiological studies of autism and related disorders.
You can watch a complete video recording of the event above. Use the comments section below to discuss the lecture and pose follow-up questions.
About the lecture:
As neutralizers of microbial agents, antibodies are major contributors to immune competence. Occasionally, however, they act as autoantibodies, which bind to a person’s own tissue, triggering autoimmune disease. In adults, the blood-brain barrier protects the brain against autoantibodies, but that barrier is not fully competent in fetuses, allowing maternal antibodies to penetrate the fetal brain and potentially alter its development. This mechanism may contribute to some cases of autism.
About the speaker:
Betty Diamond is head of the Center for Autoimmune and Musculoskeletal Diseases at the Feinstein Institute for Medical Research in New York. Her research has focused on the induction and pathogenicity of anti-DNA antibodies in systemic lupus erythematosus. She received the American College of Rheumatology’s Distinguished Investigator Award in 2001, the Lee C. Howley Sr. Prize from the Arthritis Foundation in 2002, and the Recognition Award from the National Association of M.D.-Ph.D. Programs in 2004. Diamond was elected to the Institute of Medicine in 2006.
About the commentator:
Alan S. Brown is professor of psychiatry and epidemiology at Columbia University and director of the Unit in Birth Cohort Studies at the New York State Psychiatric Institute. His research has focused on prenatal exposure to infectious, immunologic, nutritional and toxic factors, and its association with risk of schizophrenia, bipolar disorder and autism. He demonstrated earlier this year that elevated maternal C-reactive protein, an inflammatory biomarker, is related to a significantly increased risk of autism in the child. He is leading large, multi-site national birth cohort studies of prenatal biomarkers, developmental pathways and familial vulnerability based on an archived biobank and nationwide registries in Finland.

New genetic insights into autism
2013-04-25 17:00 - 18:15 | Gerald D. Fischbach Auditorium, 160 5th Avenue, New York, NY, 10010, United States
On 25 April 2013, Matthew State reviewed the genetic discoveries made over the past several years in autism research and addressed challenges in the path forward — from reliable gene discovery to an actionable understanding of the disorder’s molecular underpinnings.The talk is part of SFARI’s Autism: Emerging Concepts lecture series. You can watch a complete video recording of the event above. Use the comments section below to discuss the lecture and pose follow-up questions.
About the lecture:
The genetics of autism has reached a tipping point. The recent focus on de novo mutations — or genetic variations not passed on from either parent — has led to systematic, highly productive gene discovery efforts. This work has begun to clarify a tremendously heterogeneous genetic architecture as well as to reveal specific genes contributing to social disability syndromes.
About the speaker:
Matthew State received his undergraduate and medical degrees from Stanford University and completed his residency in psychiatry and fellowship in child psychiatry at the University of California, Los Angeles, Neuropsychiatric Institute. He received his Ph.D. in genetics from Yale University and was a faculty member there from 2001 to 2013. He is currently chair of psychiatry at the University of California, San Francisco.
State’s lab has a long-standing interest in the contribution of rare genetic mutations to childhood neuropsychiatric disorders, including autism and Tourette syndrome. He is currently leading a large, multisite, genome-wide study of autism funded by the Simons Foundation and is playing a leadership role in the Tourette International Collaborative for Genetics and the Autism Sequencing Consortium. Among many professional honors, he has been awarded the Ruane Prize for Outstanding Research in Child and Adolescent Psychiatry by the Brain and Behavior Research Foundation.
