13/03/2013 - 12:00 - Auditori PRBB

CANCELLED! Narrowing “Down” the genes: Dyrk1A as a multi-level regulator of adult plasticity

Scientific sessions, CRG Group Leader Seminars

Mara Dierssen

Systems Biology Programme, CRG


Mara Dierssen earned her M.D. and Ph.D. in Neurosciences from the University of Cantabria (UC, Spain). She started her experimental work with the electrophysiology of the Aplysia cervical ganglion and then studied the central mechanisms involved in the control of breathing using neurosurgical, pharmacological and microiontophoretic approaches. Dierssen did a postdoc at the Autonomous University of Barcelona where she focused on experimental psychology and neuropharmacology and visited the Freie Universität in Berlin to learn human neuropathology. While an assistant professor at UC, she became interested in learning and memory alterations in cognitive diseases and the influence of environment on brain neuropathology. The primary research interest of her lab is the fundamental molecular mechanisms of cognition and neural plasticity and their role in diseases of the brain. They use a multilevel approach, primarily involving neuroanatomy and behavioral neuropharmacology. The Dierssen’s lab has now joined the Systems Biology Programme at the CRG, where they will combine experimental work with computational modeling.

Talk summary

Does a thought create new synapses? Does learning a fact give rise to new brain cells in the hippocampus? The ability of the mammalian brain to change with experience is perhaps its most important feature. Why do these processes go wrong in mental illness and is there anything we can do about it? We know little about the genes that underlie the plastic response of traits to the environment, but we can learn important lessons from their perturbed functioning. Down syndrome is an excellent model case to study plasticity. Down syndrome is caused by the presence of an extra copy of the human chromosome 21 (HSA21), and thus bears one extra copy of more than 300 genes and this perturbed molecular landscape can impose limits on plasticity and regenerative capacity. At a first glance, it would not seem realistic that overexpression of a single gene gives rise to Down syndrome neural plasticity disturbances. However genes that lie in dosage-sensitive pathways, such as Dyrk1A, can play a major role in specific phenotypes and their normalization would constitute a useful therapeutic strategy. During several years we have taken various approaches from single neuron morphology to behavior, and we are naturally moving to neuronal networks. Tackling this challenge requires a data-driven computational modeling that enables us to link from effects expressed at synapses and ion channels, to their effects on the spiking neuronal activity in the network and the noise that this introduces into the system.