Eric Courchesne

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Eric Courchesne is an autism researcher and Professor of Neurosciences in University of California, San Diego School of Medicine and Director of the UCSD Autism Center located in La Jolla, California.

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Biography

Courchesne is a graduate of the University of California, where he obtained his BA in Zoology from UC Berkeley in 1970 and his PhD from UC San Diego in Neurosciences in 1975. He completed two post-doctoral appointments at Stanford University in the Departments of Psychiatry and Psychology. Courchesne contracted polio at age 3 and was initially unable to stand or walk. He has said in interviews contracting polio got him interested in neuroscience. Despite his contraction of polio, he went on to excel in gymnastics and was nominated for the Nissin Award in gymnastics, presented with the Jake Gimble Award for Scholastic and Athletic Achievement, and the National Collegiate Athletic Association (NCAA) Scholarship in the Neurosciences. He currently lives in San Diego, California with his wife, also an autism researcher, Karen Pierce, PhD, and their family. Scientifically, Courchesne’s contribution has led to over 180 publications on the topic of autism and has been included in national and international news coverage. He has received several awards such as the San Diego Health Hero Award. His research is supported by multiple organizations including the National Institute of Health, Autism Speaks, and the Simons Foundation. [1]

Scientific contributions

Courchesne made his initial major contribution to autism research in 1988 when he published one of the first neuroimaging studies of autism in the New England Journal of Medicine, demonstrating that autism involves developmental brain defects in the cerebellum and is definitively a neural biological disorder of early development and not a psychological disorder. A decade later Dr. Courchesne demonstrated that autism is also a disorder of brain growth. His 2001 Neurology paper on this topic is a landmark structural MRI paper and was republished on its 10th anniversary by Neurology because of its major impact on many subsequent studies aimed at understanding the anatomical developmental bases of autism. Courchesne’s body of research has led to the theory that autism is a disorder with a unique brain growth trajectory that includes early brain overgrowth during the toddler years, arrest of brain growth during childhood and possible degeneration during adulthood. [2] [3] [4]

In 2011, Courchesne and his colleagues discovered a 67% excess of neurons in prefrontal cortex in young males with autism and demonstrated that this excess co-occurs with excess postmortem brain weight. This finding, published in JAMA, not only helped to explain why most of all autistic 2- to 16-year-old postmortem male brains exceed normal average, but that prenatal mechanisms regulating the number of neurons may be implicated in the etiology of autism. This study thus cast doubt on the idea that autism is caused by postnatal events such as vaccines. [3] [5] [6]

Impact on society

Courchesne began in the field of autism over 30 years ago, at a time when autism was poorly understood and awareness was low at the community level. Courchesne’s major findings of cerebellar abnormalities and dysregulation of brain growth have been replicated by many independent research groups and form the foundation of many theories and research studies on autism. [1]

He continues to give lectures and keynote addresses at a variety of scientific conferences worldwide such as the International Meeting for Autism Research (IMFAR) and the Asia Pacific Autism Conference. He donates his time to the San Diego autism community and serves on the board of directors of the National Foundation for Autism Research (NFAR), an organization which supports local programs designed to improve the quality of life for individuals with autism and their families.

Publications

Related Research Articles

Reelin Large secreted extracellular matrix glycoprotein involved in neuronal migration

Reelin (RELN) is a large secreted extracellular matrix glycoprotein that helps regulate processes of neuronal migration and positioning in the developing brain by controlling cell–cell interactions. Besides this important role in early development, reelin continues to work in the adult brain. It modulates synaptic plasticity by enhancing the induction and maintenance of long-term potentiation. It also stimulates dendrite and dendritic spine development and regulates the continuing migration of neuroblasts generated in adult neurogenesis sites like the subventricular and subgranular zones. It is found not only in the brain but also in the liver, thyroid gland, adrenal gland, Fallopian tube, breast and in comparatively lower levels across a range of anatomical regions.

Transcranial magnetic stimulation Form of brain stimulation using magnetic fields

Transcranial magnetic stimulation (TMS) is a noninvasive form of brain stimulation in which a changing magnetic field is used to cause electric current at a specific area of the brain through electromagnetic induction. An electric pulse generator, or stimulator, is connected to a magnetic coil, which in turn is connected to the scalp. The stimulator generates a changing electric current within the coil which induces a magnetic field; this field then causes a second inductance of inverted electric charge within the brain itself.

V. S. Ramachandran Indian-American neuroscientist

Vilayanur Subramanian Ramachandran is an Indian-American neuroscientist. Ramachandran is known for his wide-ranging experiments and theories in behavioral neurology, including the invention of the mirror box. He is a Distinguished Professor in UCSD's Department of Psychology, where he is the director of the Center for Brain and Cognition.

Simon Baron-Cohen British psychologist and author

Sir Simon Philip Baron-Cohen is a British clinical psychologist and professor of developmental psychopathology at the University of Cambridge. He is the director of the university's Autism Research Centre and a Fellow of Trinity College. In 1985, Baron-Cohen formulated the mind-blindness theory of autism, the evidence for which he collated and published in 1995. In 1997, he formulated the fetal sex steroid theory of autism, the key test of which was published in 2015.

Mind-blindness is a concept of a cognitive divergence where an individual is unable to attribute mental states to others. As a result of this kind of social and empathetic cognitive phenomenon, the individual is incapable of putting themselves "into someone else's shoes" and cannot conceptualize, understand or predict knowledge, thoughts, beliefs, emotions, feelings, desires, behaviours, actions and intentions of another person. Such an ability to develop a mental awareness of what is in others' minds is known as the theory of mind (ToM), and the "mind-blindness" theory asserts that children who delay in this development often will develop autism. In addition to the research done on autism, ToM and mind-blindness research has recently been extended to other fields such as schizophrenia, dementia, bipolar disorders, antisocial personality disorders as well as normal aging.

Dentate nucleus Nucleus in the centre of each cerebellar hemisphere

The dentate nucleus is a cluster of neurons, or nerve cells, in the central nervous system that has a dentate – tooth-like or serrated – edge. It is located within the deep white matter of each cerebellar hemisphere, and it is the largest single structure linking the cerebellum to the rest of the brain. It is the largest and most lateral, or farthest from the midline, of the four pairs of deep cerebellar nuclei, the others being the globose and emboliform nuclei, which together are referred to as the interposed nucleus, and the fastigial nucleus. The dentate nucleus is responsible for the planning, initiation and control of voluntary movements. The dorsal region of the dentate nucleus contains output channels involved in motor function, which is the movement of skeletal muscle, while the ventral region contains output channels involved in nonmotor function, such as conscious thought and visuospatial function.

Executive functions are a set of cognitive processes that are necessary for the cognitive control of behavior: selecting and successfully monitoring behaviors that facilitate the attainment of chosen goals. Executive functions include basic cognitive processes such as attentional control, cognitive inhibition, inhibitory control, working memory, and cognitive flexibility. Higher-order executive functions require the simultaneous use of multiple basic executive functions and include planning and fluid intelligence.

Orbitofrontal cortex Region of the prefrontal cortex of the brain

The orbitofrontal cortex (OFC) is a prefrontal cortex region in the frontal lobes of the brain which is involved in the cognitive process of decision-making. In non-human primates it consists of the association cortex areas Brodmann area 11, 12 and 13; in humans it consists of Brodmann area 10, 11 and 47.

Mu wave Synchronized patterns of electrical activity in the part of the brain that controls voluntary movement

The sensorimotor mu rhythm, also known as mu wave, comb or wicket rhythms or arciform rhythms, are synchronized patterns of electrical activity involving large numbers of neurons, probably of the pyramidal type, in the part of the brain that controls voluntary movement. These patterns as measured by electroencephalography (EEG), magnetoencephalography (MEG), or electrocorticography (ECoG), repeat at a frequency of 7.5–12.5 Hz, and are most prominent when the body is physically at rest. Unlike the alpha wave, which occurs at a similar frequency over the resting visual cortex at the back of the scalp, the mu rhythm is found over the motor cortex, in a band approximately from ear to ear. A person suppresses mu rhythms when he or she performs a motor action or, with practice, when he or she visualizes performing a motor action. This suppression is called desynchronization of the wave because EEG wave forms are caused by large numbers of neurons firing in synchrony. The mu rhythm is even suppressed when one observes another person performing a motor action or an abstract motion with biological characteristics. Researchers such as V. S. Ramachandran and colleagues have suggested that this is a sign that the mirror neuron system is involved in mu rhythm suppression, although others disagree.

Manuel Casanova

Manuel F. Casanova is the SmartState Endowed Chair in Childhood Neurotherapeutics and a professor of Biomedical Sciences at the University of South Carolina School of Medicine Greenville. He is a former Gottfried and Gisela Kolb Endowed Chair in Outpatient Psychiatry and a Professor of Anatomical Sciences and Neurobiology at the University of Louisville.

Reward system Group of neural structures responsible for motivation and desire

The reward system is a group of neural structures responsible for incentive salience, associative learning, and positively-valenced emotions, particularly ones involving pleasure as a core component. Reward is the attractive and motivational property of a stimulus that induces appetitive behavior, also known as approach behavior, and consummatory behavior. A rewarding stimulus has been described as "any stimulus, object, event, activity, or situation that has the potential to make us approach and consume it is by definition a reward". In operant conditioning, rewarding stimuli function as positive reinforcers; however, the converse statement also holds true: positive reinforcers are rewarding.

TSHZ3

Teashirt homolog 3 is a protein that in humans is encoded by the TSHZ3 gene. In mice, it is a necessary part of the neural circuitry that controls breathing. The gene is also a homolog of the Drosophila melanogaster teashirt gene, which encodes a zinc finger transcription factor important for development of the trunk.

Nancy Minshew is a Professor of Psychiatry and Neurology at the University of Pittsburgh. She directs the Center of Excellence in Autism Research and is an internationally known expert in the cognitive, neurological, and genetic bases of autism. Minshew was trained as a behavioral child neurologist, and she received an M.D. from the Washington University School of Medicine in St. Louis.

Gyrification is the process of forming the characteristic folds of the cerebral cortex. The peak of such a fold is called a gyrus, and its trough is called a sulcus. The neurons of the cerebral cortex reside in a thin layer of gray matter, only 2–4 mm thick, at the surface of the brain. Much of the interior volume is occupied by white matter, which consists of long axonal projections to and from the cortical neurons residing near the surface. Gyrification allows a larger cortical surface area and hence greater cognitive functionality to fit inside a smaller cranium. In most mammals, gyrification begins during fetal development. Primates, cetaceans, and ungulates have extensive cortical gyri, with a few species exceptions, while rodents generally have none. Gyrification in some animals, for example the ferret, continues well into postnatal life.

Neurogenomics

Neurogenomics is the study of how the genome of an organism influences the development and function of its nervous system. This field intends to unite functional genomics and neurobiology in order to understand the nervous system as a whole from a genomic perspective.

Autism spectrum Range of neurodevelopmental disorders

The autism spectrum encompasses a range of neurodevelopmental conditions, including autism and Asperger syndrome, generally known as autism spectrum disorders (ASD). Individuals on the autism spectrum typically experience difficulties with social communication and interaction and may also exhibit restricted, repetitive patterns of behavior, interests, or activities. Symptoms are typically recognized between one and two years of age in boys. However, many children are not diagnosed until they are older. It is also common for diagnosis to be received as an adolescent or as an adult. The term "spectrum" refers to the variation in the type and severity of symptoms. Those in the mild range are typically able to function independently, with some difficulties, while those with moderate to severe symptoms may require more substantial support in their daily lives. Long-term problems may include difficulties in daily living such as managing schedules, hypersensitivities, creating and keeping relationships, and maintaining jobs.

Cerebellar cognitive affective syndrome (CCAS), also called Schmahmann's syndrome is a condition that follows from lesions (damage) to the cerebellum of the brain. It refers to a constellation of deficits in the cognitive domains of executive function, spatial cognition, language, and affect resulting from damage to the cerebellum. Impairments of executive function include problems with planning, set-shifting, abstract reasoning, verbal fluency, and working memory, and there is often perseveration, distractibility and inattention. Language problems include dysprosodia, agrammatism and mild anomia. Deficits in spatial cognition produce visual–spatial disorganization and impaired visual–spatial memory. Personality changes manifest as blunting of affect or disinhibited and inappropriate behavior. These cognitive impairments result in an overall lowering of intellectual function. CCAS challenges the traditional view of the cerebellum being responsible solely for regulation of motor functions. It is now thought that the cerebellum is responsible for monitoring both motor and nonmotor functions. The nonmotor deficits described in CCAS are believed to be caused by dysfunction in cerebellar connections to the cerebral cortex and limbic system.

The development of an animal model of autism is one approach researchers use to study potential causes of autism. Given the complexity of autism and its etiology, researchers often focus only on single features of autism when using animal models.

Cajal–Retzius cells are a heterogeneous population of morphologically and molecularly distinct reelin-producing cell types in the marginal zone/layer I of the developmental cerebral cortex and in the immature hippocampus of different species and at different times during embryogenesis and postnatal life.

Autism's symptoms result from maturation-related changes in various systems of the brain. How autism occurs is not well understood. Its mechanism can be divided into two areas: the pathophysiology of brain structures and processes associated with autism, and the neuropsychological linkages between brain structures and behaviors. The behaviors appear to have multiple pathophysiologies.

References

  1. 1 2 Zimmer, Carl. "The Brain: The Troublesome Bloom of Autism". Discover Magazine. Retrieved 20 April 2013.
  2. Robbins, Gary. "UCSD finds genes possibly linked to autism". San Diego Union-Tribune. Retrieved 20 April 2013.
  3. 1 2 Jabr, Ferris. "The Ballooning Brain: Defective Genes May Explain Uncontrolled Brain Growth in Autism". Scientific American. Retrieved 20 April 2013.
  4. "Excess of Neurons in Prefrontal Cortex Associated with Autism". Scicasts. Retrieved 20 April 2013.
  5. Park, Alice (9 November 2011). "Autistic Children Have More Brain Cells". Time. Retrieved 20 April 2013.
  6. Goodwin, Jennifer (8 November 2011). "Autistic children may have too many brain cells, study says". USA Today. Retrieved 20 April 2013.