boston-neurotalks : Messages : 5910-5939 of 5939

Has Brain Imaging Discovered Anything New? · 5910 - 5939

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The Autism and Developmental Disorders Colloquium Series at MIT

"Functional imaging of social communication deficits in autism and relation to
autism risk genes"

Susan Bookheimer, Ph.D.
Joaquin Fuster Professor  of Cognitive Neurosciences, Department of Psychiatry
and Biobehavioral Sciences,
UCLA School of Medicine

6:00 p.m., Wednesday, November 18, 2009
MIT Building 46-3002 (auditorium), followed by a reception
Building Address:  43 Vassar Street, Cambridge, MA  02139

Hosted by Nancy Kanwisher, Ph.D., Walter A. Rosenblith Professor of Cognitive
Neuroscience, Department of Brain and Cognitive Sciences at MIT

Please RSVP to lmavros@...

This talk will present several functional MRI studies of children with autism
that examine critical aspects of the autism spectrum, particularly those
involved with social communication. Data from artificial language acquisition,
implicit learning, reward responsiveness, and imitation/observation of affect,
suggest a relatively circumscribed network of brain regions consistently
affected in autism. I will argue that a primary deficit in striatal mediated
reward systems underlies the social motivation deficit in autism, affecting
implicit learning systems involved in language acquisition and social skills
development. The relationship between abnormalities in these brain regions and
autism risk genes will also be presented.

Supported by the Simons Initiative on Autism and the Brain at MIT
(web.mit.edu/autism)

________________________________________________________________

The Autism and Developmental Disorders Colloquium Series at MIT

"Autism: What we know? What we need?"

Thomas R. Insel, MD
National Institute of Mental Health, NIH
Bethesda, MD, USA

6:00 p.m., Wednesday, December 2, 2009
MIT Building 46-3002 (auditorium), followed by a reception
Building Address:  43 Vassar Street, Cambridge, MA  02139

Hosted by Mriganka Sur, Ph.D., Sherman Fairchild Professor of Neuroscience
Head, Department of Brain and Cognitive Sciences at MIT

Please RSVP to lmavros@...

Since the first description by Leo Kanner more than 60 years ago, autism has
become a broad clinical construct with intense public and scientific interest.
According to a recent article in the New York Times, ?autism has become to
disorders what Africa is to social issues.? (April 27, 2007) This talk will
attempt to summarize what we know and what we need to know in 2009.  We know
that autism can be studied as a developmental brain disorder, likely due to
synaptic dysfunction.  We need to know more about the precise nature or
location of this dysfunction, beyond recognizing that diverse cortical pathways
appear to be involved. We know from twin studies that autism is heritable and
that several Mendelian disorders are associated with autism.  Genetic studies
of autism conform to a complex pattern, including highly penetrant rare
mutations as well as less penetrant common risk alleles.   While the genetics
of autism has matured rapidly, we still need to use genetics as a portal to
pathophysiology, ultimately identifying molecular pathways for treatment
targets.    We know that the prevalence of autism has increased markedly, but
we do not know if this increasing prevalence has been matched by increasing
incidence.  We need to know if there are specific environmental changes
contributing to the increasing prevalence or if it is mostly ascertainment
factors that are driving this dramatic rise in autism.   Perhaps our greatest
certainty is that autism spectrum disorder, as it is described today, is a
highly heterogeneous collection of developmental disorders, likely as
heterogeneous as seizure disorders or mental retardation. Much confusion, both
in research and practice, stems from our inability to identify the many
syndromes within the autism spectrum, syndromes that differ in cause, treatment
response, and prognosis.  We need a much clearer picture of the subtypes of
autism to facilitate research progress and optimize diagnosis and treatment.

Supported by the Simons Initiative on Autism and the Brain at MIT
(web.mit.edu/autism)
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-----Original Message-----
From: owner-cmbseminar-list@... [mailto:owner-cmbseminar-list@...] On
Behalf Of Denise Parisi
Sent: Monday, November 16, 2009 3:41 PM
To: undisclosed-recipients:
Subject: Tuesday, November 17th, 1:00PM - Vision Colloquium - Jeffrey Y.
Lin, University of Washington

*Department of Psychology*

*Brain, Behavior and Cognition (BBC) Program *

*/Introduces /*

*Vision Colloquium Series*

** * ****

*First Speaker of the Series*

** * **

*Jeffrey Y. Lin*

Department of Psychology, Cognition & Perception

(Geoffrey Boynton Lab)

University of Washington

Tuesday, November 17, 2009

1:00-2:00PM

Room 150, 64 Cummington Street, Boston, MA 02215

*/Perception in the Absence of Awareness/*

Visual spatial attention is typically associated with conscious visual
awareness.  However, we will show in two separate studies that this is
not always the case.

In the first study we show that attention can be automatically drawn
toward a stimulus, even when the stimulus is perceptually
indistinguishable from a stimulus that does not attract attention.
Specifically, we show that a looming stimulus on a collision path with
an observer captures attention (as measured in a visual search task) but
a looming stimulus on a near-miss path does not. Critically, the two
motion stimuli had nearly identical motion trajectories and observers
were unaware of the differences between collision and near-miss stimuli
even when explicitly asked to discriminate between them in a separate
experiment.

In the second study we show that information is automatically encoded
outside the spatial focus of attention at behaviorally relevant points
in time. Subjects performed an RSVP task at fixation while a sequence of
natural scenes was placed in the background. In a subsequent memory
task, only the scene presented coincidentally with the target in the
RSVP task was recalled above chance, as though the entire visual scene
was captured at the time of target detection. Surprisingly, subjects
were unaware of this enhanced performance and felt that they were guessing.

Together, these studies show that conscious visual awareness is not
necessary for a stimulus to (1) attract visual attention and (2) become
encoded into memory.

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HRC seminars resumes in the fall semester. HRC talks are scheduled on
Friday mornings from 10:30 --noon @ Rm 203, 44 Cummington St.
Refreshments will be provided. Like always, if you want to give a
seminar or if you want to see someone invited, please do not hesitate
to contact us at konglqcns@.... The event calendar of the HRC
talks could be found at http://www.bu.edu/hrc/news/ .

==================================================
Friday, Nov. 20, 2009
10:30AM - 12:00PM
44 Cummington st. Rm 203

Prof. PETER CARIANI
Department of Otology and Laryngology, Harvard Medical School
Title: Auditory and Visual Sensations: Yoichi Ando's theory of
architectural acoustics

ABSTRACT

Professor Yoichi Ando, is a well-known architectural acoustician who
designed the Kirishima International Concert Hall in Japan. His design
method used genetic algorithms to optimize the acoustics according to
the psychophysics of listener preferences.  I served as guest editor
for his most recent book on architectural acoustics and perception,
which has just been published by Springer this month. The book
summarizes decades of psychophysical experiments related to auditory
perception and listener preferences as well as neurophysiological
observations (ABR, SVR, EEG, MEG) of their neural correlates that were
made by Ando and his colleagues. I will give an overview of Ando's
psychophysics-based approach to architectural acoustics, their
psychophysical and neurophysiological findings, and his
correlation-based theory of hearing and vision. Ando proposes a
correlation-based model of neuronal signal processing in which
features of an internal autocorrelation representation subserve
"temporal sensations" (pitch, timbre, loudness, duration) while
features of an internal interaural crosscorrelation representation
subserve "spatial sensations" (sound location, size, diffuseness
related to envelopment). Together these two representations account
for the basic auditory qualities that are relevant for listening to
music and speech in indoor performance spaces. Remarkably, Ando and
colleagues have found many visual analogues of auditory percepts and
preferences (e.g. missing fundamental of flickering light, preferences
for flickering lights, oscillatory movements, texture regularity).

===================================================
Scheduled Future Seminars:

Dec. 4.  Prof. Judy Dubno

Dec. 11. Dr. Courtenay Wilson

Jan. 8, 2010 Dr. Mitch Day

Jan. 22, 2010, Prof. George Pollak and Dr.Josh Gittleman

April.23, 2010 Prof. Mark Chertoff

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TODAY 11/18 at noon
Seminar room 2204
149 13th St., Charlestown Navy Yard

Frank Guenther, Ph.D.
Professor, Department of Cognitive and Neural Systems,
Boston University, MA

Title: The neural control of speech

Abstract:
Speech production involves coordinated processing in many regions of
the brain. To better understand these processes, our laboratory has
designed, tested, and iteratively refined a neural network model whose
components correspond to brain regions involved in speech. Babbling
and imitation phases are used to train neural mappings between
phonological, articulatory, auditory, and somatosensory
representations. After learning, the model can produce syllables and
words it has learned by commanding movements of an articulatory
synthesizer. Because the model�s components correspond to neurons and
are given precise anatomical locations, activity in the model�s cells
can be compared to neuroimaging data. Computer simulations of the
model account for a wide range of experimental findings, including
data on acquisition of speaking skills, articulatory kinematics, and
brain activity during normal and perturbed speech. Furthermore,
�damaged� versions of the model are being used to investigate a number
of communication disorders, including stuttering, apraxia of speech,
and spasmodic dysphonia. Finally, the model has been used to guide
development of a brain-machine interface (BMI) aimed at restoring
speech output to profoundly paralyzed individuals. A volunteer
suffering from locked-in syndrome was able to use the BMI to control
movements of a speech synthesizer in order to produce vowel sounds,
reaching a level of 70% accuracy after 5-10 practice attempts of each
vowel sound. These results were obtained from a single cone electrode
with only two input channels; significant improvements in performance
are expected in future systems utilizing more electrodes and optimized
synthesizers.

------------------------------------------------------
Adrian KC Lee, ScD
Martinos Center for Biomedical Imaging
149 13th St., Suite 2301
Charlestown, MA 02129
Tel: 617-726-8791
Fax: 617-726-7422

Brainmap Website:
http://nmr.mgh.harvard.edu/martinos/training/brainMap_2009-2010.php

The Autism and Developmental Disorders Colloquium Series at MIT

"Functional imaging of social communication deficits in autism and relation to
autism risk genes"

Susan Bookheimer, Ph.D.
Joaquin Fuster Professor  of Cognitive Neurosciences, Department of Psychiatry
and Biobehavioral Sciences,
UCLA School of Medicine

6:00 p.m., Wednesday, November 18, 2009
MIT Building 46-3002 (auditorium), followed by a reception
Building Address:  43 Vassar Street, Cambridge, MA  02139

Hosted by Nancy Kanwisher, Ph.D., Walter A. Rosenblith Professor of Cognitive
Neuroscience, Department of Brain and Cognitive Sciences at MIT

Please RSVP to lmavros@...

This talk will present several functional MRI studies of children with autism
that examine critical aspects of the autism spectrum, particularly those
involved with social communication. Data from artificial language acquisition,
implicit learning, reward responsiveness, and imitation/observation of affect,
suggest a relatively circumscribed network of brain regions consistently
affected in autism. I will argue that a primary deficit in striatal mediated
reward systems underlies the social motivation deficit in autism, affecting
implicit learning systems involved in language acquisition and social skills
development. The relationship between abnormalities in these brain regions and
autism risk genes will also be presented.

Supported by the Simons Initiative on Autism and the Brain at MIT
(web.mit.edu/autism)
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Title: The visual experience of the human infant: normal and abnormal
Speaker: T. Rowan Candy, MCOptom, Ph.D. Indiana University School of Optometry
Location: Schepens Eye Research Institute, 20 Staniford Street, Boston

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Dr. Bodfish's talk will be on Wednesday, December 16th.
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The Autism and Developmental Disorders Colloquium Series at MIT

"Autism: What we know? What we need?"

Thomas R. Insel, MD
National Institute of Mental Health, NIH
Bethesda, MD, USA

6:00 p.m., Wednesday, December 2, 2009
MIT Building 46-3002 (auditorium), followed by a reception
Building Address:  43 Vassar Street, Cambridge, MA  02139

Hosted by Mriganka Sur, Ph.D., Sherman Fairchild Professor of Neuroscience
Head, Department of Brain and Cognitive Sciences at MIT

Please RSVP to lmavros@...

Since the first description by Leo Kanner more than 60 years ago, autism has
become a broad clinical construct with intense public and scientific interest.
According to a recent article in the New York Times, ?autism has become to
disorders what Africa is to social issues.? (April 27, 2007) This talk will
attempt to summarize what we know and what we need to know in 2009.  We know
that autism can be studied as a developmental brain disorder, likely due to
synaptic dysfunction.  We need to know more about the precise nature or
location of this dysfunction, beyond recognizing that diverse cortical pathways
appear to be involved. We know from twin studies that autism is heritable and
that several Mendelian disorders are associated with autism.  Genetic studies
of autism conform to a complex pattern, including highly penetrant rare
mutations as well as less penetrant common risk alleles.   While the genetics
of autism has matured rapidly, we still need to use genetics as a portal to
pathophysiology, ultimately identifying molecular pathways for treatment
targets.    We know that the prevalence of autism has increased markedly, but
we do not know if this increasing prevalence has been matched by increasing
incidence.  We need to know if there are specific environmental changes
contributing to the increasing prevalence or if it is mostly ascertainment
factors that are driving this dramatic rise in autism.   Perhaps our greatest
certainty is that autism spectrum disorder, as it is described today, is a
highly heterogeneous collection of developmental disorders, likely as
heterogeneous as seizure disorders or mental retardation. Much confusion, both
in research and practice, stems from our inability to identify the many
syndromes within the autism spectrum, syndromes that differ in cause, treatment
response, and prognosis.  We need a much clearer picture of the subtypes of
autism to facilitate research progress and optimize diagnosis and treatment.

Supported by the Simons Initiative on Autism and the Brain at MIT
(web.mit.edu/autism)

___________________________________________________________________________

The Autism and Developmental Disorders Colloquium Series at MIT

"A role for interests and reward in the pathogenesis and treatment of autism"

Jim Bodfish, Ph.D.
Thomas E. Castelloe Distinguished Professor of Pediatrics and Psychiatry
Carolina Institute for Developmental Disabilities, University of North Carolina
at Chapel Hill

6:00 p.m., Wednesday, December 18, 2009
MIT Building 46-3002 (auditorium), followed by a reception
Building Address:  43 Vassar Street, Cambridge, MA  02139

Hosted by Jill Crittenden, Ph.D., Research Scientist, McGovern Institute for
Brain Research and Center for Cancer Research, Massachusetts Institute of
Technology

Please RSVP to lmavros@...

In recent studies we have found that so called "Circumscribed Interests" (CI)
can be isolated as a discrete subtype of repetitive behavior, appear to be
familial, and appear to impart significant added impairment in autism over and
above other core (social, communication) and associated (cognitive) deficits.
CI present in idiosyncratic ways across cases but all involve a heightened
interest in and restricted activity with circumscribed nonsocial aspects of the
environment and experience.  The heightened interest and restricted focus that
is characteristic of CI suggest that cognitive-affective processes that mediate
reward may be altered in persons with autism.  We hypothesize that the
development of CI in autism is mediated by an underlying cognitive-affective
reward system that is "biased" away from social information and towards
nonsocial information. If supported this model may help explain how social
deficits and excessive repetitive behaviors come to co-occur in autism.
Further, it could be used to guide research on autism pathogenesis and
treatment. In this talk I will discuss our research on the phenomenology and
neural circuitry associated with CI, and our translational studies of CI in a
mouse model designed for high through-put screening of potential pharmacologic
treatments.

Supported by the Simons Initiative on Autism and the Brain at MIT
(web.mit.edu/autism)
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HRC seminars resumes in the fall semester. HRC talks are scheduled on
Friday mornings from 10:30 --noon @ Rm 203, 44 Cummington St.
Refreshments will be provided. Like always, if you want to give a
seminar or if you want to see someone invited, please do not hesitate
to contact us at konglqcns@.... The event calendar of the HRC
talks could be found at http://www.bu.edu/hrc/news/ .

==================================================
Friday, Nov. 27, 2009
10:30AM - 12:00PM
44 Cummington st. Rm 203

NO HRC seminar this Friday.

HAPPY THANKSGIVING TO ALL!

===================================================
Scheduled Future Seminars:

Dec. 4.  Prof. Judy Dubno

Dec. 11. Dr. Courtenay Wilson

Jan. 8, 2010 Dr. Mitch Day

Jan. 22, 2010, Prof. George Pollak and Dr.Josh Gittleman

April.23, 2010 Prof. Mark Chertoff

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