Theresa Harrison

BRI member leads study showing how a molecular receptor helps restore brain function after 'silent stroke'

S. Thomas Carmichael, M.D., Ph.D., professor of neurology at the David Geffen School of Medicine, is senior author of a five year study that shows how the brain can be repaired and brain function recovered after a stroke in animals.

The discovery could have important implications for treating a mind-robbing condition known as a white matter stroke, which is a major form of dementia. "Despite how common and devastating white matter stroke is, there has been little understanding of how the brain responds and if it can recover," Dr. Carmichael said. "By studying the mechanisms and limitations of brain repair in this type of stroke, we will be able to identify new therapies to prevent disease progression and enhance recovery."

The study was published in the Proceedings of the National Academy of Sciences (December 27th, 2016).

More details here.

Image left: New brain cells replace those destroyed by stroke in animals: immature cells are green, more mature cells are red and fully mature cells are orange.


June Image of the Month

Image of the Month

Traverse section of day 4 chicken embryo labeled with antibodies against Lhx2/9 (red), IsI1I (green), and LhxI/5 (blue). These transcription factors are establishing both different classes of neurons in the spinal cord and distinct mesodermal derivatives in the proximal distal limb and embryonic kidneys.


Image by Madeline Andrews from the laboratory of Samantha Butler, Ph.D.





In the News Image

Announcing the Inaugural Recipients of the BRI Knaub Fellowship in Multiple Sclerosis Research 

Funded by a generous gift from the Knaub Unitrust, established by Richard and Suzanne Knaub, the fellowships support Postdoctoral or Predoctoral Fellows pursuing projects related to Multiple Sclerosis research at UCLA. The fellowships recognize young scientists who exemplify trainee excellence, innovation, and a multidisciplinary approach to MS research. 

The inaugural Knaub Fellows are Stefano Lepore, Ph.D. from the laboratory of Allan Mackenzie-Graham, Ph.D.; and David DiTullio from the laboratory of S. Thomas Carmichael, M.D., Ph.D. 

"We want to express our sincere gratitude to the Knaub family for this generous gift which will enable these young researchers to contribute to translational research related to understanding and treating MS," said BRI Director Christopher Evans.

Learn more about the 2017 Knaub Fellows here.



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Joint Seminars in Neuroscience Lecture Series

Tuesday, January 17, 2017

Dr. Jessica Cardin, Ph.D.
Assistant Professor of Neuroscience
Department of Neuroscience and Kavli Institute for Neuroscience
Yale University School of Medicine
New Haven, CT

"Cortical Function and Dysfunction: A Role for Dendrite Targeting Interneurons in Cortical Development and Disease"

Current evidence suggests that dysregulation of GABAergic interneurons contributes to neural and behavioral deficits in several neurodevelopmental disorders, including schizophrenia.  However, there are multiple populations of interneurons and their respective roles in psychiatric disease remain poorly explored.  Neuregulin 1 (NRG1) and its interneuron-specific tyrosine kinase receptor ERBB4 are risk genes for schizophrenia, and the Nrg1/ErbB4 pathway is important for normal cortical development.  Using a conditional ErbB4 deletion model, we directly tested the role of vasoactive intestinal peptide (VIP)-expressing interneurons in schizophrenia-related deficits in vivo.  ErbB4 removal from VIP interneurons during development leads to changes in their activity, along with severe dysregulation of the temporal organization and state-dependence of cortical activity.  As a result of these neural circuit alterations, animals in which VIP interneurons lack ErbB4 exhibit behavioral abnormalities, reduced cortical responses to sensory stimuli, and impaired sensory learning.  Our data support a key role for VIP interneurons in normal cortical circuit development and suggest that their disruption contributes to pathophysiology in the ErbB4 model of schizophrenia.  These findings provide a new perspective on the fold of GABAergic interneuron diversity in the disruption of cortical function in complex psychiatric diseases.

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