MC02 - Molecular basis for synaptic function highlighting disease mechanisms - Organised by European Society for Neurochemistry (ESN) (09:00-15:00)

There are currently hardly any disease modifying treatments for neurodevelopmental or
neurodegenerative diseases presenting malfunctioning synaptic connections. Our Mini-Conference will
highlight novel aspects of genes and behavior toward better therapeutics.
Last year, the Autism Sequencing Consortium published the largest autism spectrum disorder (ASD)
exome sequencing to date, revealing 102 candidate genes and suggesting that ASD must arise by
phenotypic convergence among diverse origins. In other words, common molecular pathways may
explain the apparently diverse genomic landscape behind ASD. In line with this hypothesis, our Mini-
Conference addresses recent work to bridge the nature of this convergence and brings together a group
of scientists who are studying the molecular, cellular and synaptic disruptions caused by mutations in
genes associated with ASD. Additional disease mechanisms inflicting synapse function, such as
protein mis-folding, mitochondrial activity, lipid rafts and gene regulation will be addressed with
converging and disparate mechanisms.

Chair: Illana Gozes, ESN Secretary

Organizing Committee: Johannes Hirrlinger, ESN President, Carlos Duarte, ESN Treasurer,
Natalia N. Nalivaeva, ESN Past President

Patricia Monteiro, Portugal – SHANK proteins: roles at the synapse and in autism
spectrum disorder
Illana Gozes, Israel – Essential for the synapse: ADNP a major regulator of development and aging
Julien Courchet, France – Fine-tuning of cortical circuits development through a local
regulation of mitochondrial metabolism
Angelo Poletti, Italy – Protein misfolding in motor neuron diseases
Sara Grassi, Italy – Lipid rafts in neurodegeneration and neuroprotection
Natalia N. Nalivaeva, UK, Russia – Prenatal stress and neuronal gene regulation

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