IPSEN Prize for Neuronal Plasticity awarded to Professor David Porteous

The Fondation IPSEN ‘Neuronal Plasticity Prize’ has been awarded annually since 1990. The Jury highlights a field of neuroscience and typically three Laureates are recognised: July 2015

La Fondation IPSEN highlights fundamental advances in biomedical research and clinical medicine, identifying emerging knowledge and new paradigms, and facilitates the process of interdisciplinary cross-fertilisation between research domains. The Fondation IPSEN ‘Neuronal Plasticity Prize’ has been awarded annually since 1990. The Jury highlights a field of neuroscience and typically three Laureates are recognised. The awards were presented jointly to David Porteous, Thomas Bourgeron and Mark Bear at a packed IPSEN Foundation symposium at the 9th World Congress of the International Brain Research Organisation, Rio de Janeiro, Brazil, July 2015.

CGEM’s Head of Medical Genetics, Professor David Porteous, was recognised for his discovery of the DISC1 gene in a large Scottish family at high risk of schizophrenia, bipolar disorder or recurrent major depressive disorder, forcing a rethink on the underlying biology of these disorders. DISC1 is a scaffold protein that orchestrates the trafficking, compartition and activity of multiple neurodevelopmental and neurosignalling proteins.

Sharing the prize were:

Thomas Bourgeron for his pioneering work on identifying single gene mutations that cause autism: Neuroligin-3, neuroligin-4 and SHANK3 are all involved in synapse function. This approach has been developed by Bourgeron and picked up by others to help push autism research forward. Autism research, until recently considered a back-water, is now on the front foot of psychiatric genetics research.

Mark Bear for his pioneering work on Fragile X Syndrome, a major cause of intellectual disability due to silencing of the FMR1 gene. Bear showed that a downstream consequence of this silencing is upregulation of mGLUR5-mediated synaptic plasticity. Laboratory and now clinical studies suggest that modulation of mGLUR5 activity may have therapeutic potential for what has previously been considered an irreversible neurodevelopmental disorder.