Autism Research lectures are open to the public and are held at the Gerald D. Fischbach Auditorium at the Simons Foundation headquarters in New York City. Tea is served prior to each lecture.
In this talk, Nancy Kanwisher will consider the functional architecture of the social brain in typical subjects as an avenue for considering which functions are affected and which are preserved in autism.
Although most people regularly tune up their cars, you probably haven’t needed to bring your brain in for a tune-up, despite the fact that the human brain is far more complex than the internal combustion engine. What’s more, unlike most machines, your brain is constantly changing in order to store memories and adapt to a fluid environment. Our brains are faced with a fundamental challenge: They must preserve the integrity of the neural circuits that subserve behaviors over the lifetime of an organism, while at the same time allowing plastic mechanisms to shape and fine-tune their function.
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. Gail Mandel investigates the basis of this phenomenon and has identified cell-cell interactions between neurons and glia involved in pathological states of brain development. Mandel has ameliorated the neuropathology of one autism spectrum disorder, Rett syndrome, by genetically replacing the defective MeCP2 gene with a good copy of the gene in astrocytes – glia cells in the brain. She is now exploring the underlying mechanisms crucial for neuronal signaling.
Advances in molecular genetics have implicated a variety of genetic variations in autism, yet understanding of what these variations mean is still limited. Advances in classification of diseases have made autism among the most reliably diagnosed neurodevelopmental or neuropsychiatric disorders. But symptoms used to define autism are likely outcomes of earlier disruptions in normative social and communication development rather than causally linked to genetic perturbations.
While autism clearly involves altered function of the central nervous system, the neuropathology of the disorder remains controversial. This is due in part,to the enormous complexity of the disorder, which likely has many causes and many biological trajectories. It is also due to the fact that few neuroimaging studies involve very young children or severely affected individuals. This lack of information is compounded by the fact that findings at the magnetic resonance imaging (MRI) level of analysis cannot be confirmed and extended to the cellular level due to a lack of postmortem brains.
Burgeoning evidence shows that in typical development, the ability to structure actions according to intentions emerges during infancy. And recent evidence reveals that infancy is a period of rapid change and development in this ability. Early social knowledge depends critically on infants’ active engagement with the physical and social world.